In the far reaches of the Texas Panhandle, the 6,440-acre Muleshoe National Wildlife Refuge has been a quiet sanctuary for decades. Outdoor enthusiasts are drawn to its remote beauty, where rugged swaths of wildflowers and mesquite trees shelter the elusive pronghorn antelope and the lesser prairie chicken. Every winter, birders descend on the reserve to witness the skies above the southern High Plains churn with formations of sandhill cranes, making pit stops at the region’s shallow playa lakes. 

The state’s oldest wildlife refuge has become the latest flash point in a battle between conservation efforts and the Trump administration’s push for expanded domestic energy development. Last month, the U.S. Fish and Wildlife Service announced it was scrapping a major expansion plan for the refuge some fifteen years in the making, which would have grown it by up to 700,000 acres through voluntary conservation-easement agreements with local property owners.

Established in 1935 by President Franklin D. Roosevelt, Muleshoe was created as a winter haven for waterfowl drawn by the area’s unique saline lakes along their annual migratory route between Canada and Mexico. Today it hosts one of the world’s largest annual gatherings of sandhill cranes, with numbers reaching into the thousands. The Fish and Wildlife Service unveiled the expansion proposal in 2022, as the refuge faced shrinking wildlife populations and growing threats to natural habitats from oil and mineral extraction.

In another move, last week a federal judge in Texas ruled there had been “serious error” in the agency’s classification of the lesser prairie chicken’s endangered status, temporarily removing Endangered Species Act protections for the bird in the state—a culmination of a Republican-backed effort that began in 2023 when Attorney General Ken Paxton filed a suit to overturn the listing. Muleshoe National Wildlife Refuge has served as an important home for the prairie chicken’s dwindling population; an environmental assessment for the refuge deemed it critical to preserving the bird’s habitat. A spokesperson with the Fish and Wildlife Service told Texas Monthly the agency “remains committed to working with our partners to conserve the lesser prairie chicken and its grassland habitats.”

The move to scrap the refuge’s expansion was unprecedented, seemingly marking the first time the agency has ever withdrawn a land-protection plan. Conservation groups were quick to condemn the move, pointing to more than a decade of scientific research that went into the proposed expansion, which was intended to strengthen protections for the refuge and connect habitats hosting vulnerable species. 

“I’ve worked on refuge expansions and new designations my entire career, twenty years, and the U.S. Fish and Wildlife Service doesn’t take that on lightly,” says Desirée Sorenson-Groves, president of the National Wildlife Refuge System. “It takes years of work and building consensus with local landowners.”

Texas Republican lawmakers long opposed the conservation plan. In an August 20 statement following a visit to Muleshoe, Congressman Jodey Arrington of Lubbock cast the decision to cancel the expansion as a victory over a “ridiculous land grab” from the Biden era. He had previously moved to shut down the plan, claiming it was a misuse of taxpayer revenue and that landowners might be “coerced” into selling. In 2024 he slipped an amendment into the Department of the Interior budget bill aiming to curtail Land and Water Conservation Fund money—cash the Fish and Wildlife Service would need to buy conservation easements from willing landowners. Days after President Trump returned to the White House, in January 2025, Arrington doubled down, introducing the No FED in West Texas Act, House Resolution 839, to permanently block the expansion plan. It quickly became a rallying cry for Republican lawmakers and was championed as a struggle for private-property rights (less than 2 percent of Texas land is federally owned, according to a 2012 report). By late July his bill had cleared a key House committee—just before the agency scrapped the plan.

“Rep. Arrington’s opposition to Muleshoe was mostly, if not entirely, based in misinformation. The issue about the idea that landowners are somehow going to be forced or pressured to sell their land is simply not true,” says Nathan Marcy, a senior policy analyst at the conservation nonprofit Defenders of Wildlife.

Arrington’s office did not respond to questions about evidence before publication. In a video posted to X on Wednesday, the congressman praised the service’s cancellation of the plan.

California Democrat and House Committee on Natural Resources ranking member Jared Huffman further criticized the bill, saying in a statement, “The Land Protection Plan is entirely voluntary. It offers a new market opportunity for willing landowners . . . and helps restore one of the most threatened ecosystems on Earth: our native grasslands. But Republicans want to shut it down. . . . This bill puts politics over science, ideology over economics, and government control over private property.”

The Fish and Wildlife Service said part of the reason for the plan’s cancellation was to comply with Trump’s “Unleashing American Energy” executive order, a directive aimed at undoing Biden-era efforts to combat climate change and instead ramping up domestic production of oil, gas, and coal. Muleshoe was one of the few remaining vestiges of the Biden administration’s “America the Beautiful” initiative, which aimed to conserve at least 30 percent of U.S. lands and waters by 2030. The initiative established four new refuges in the National Wildlife Refuge System during its tenure.

Arrington’s claim to be defending private-property owners stands in stark contrast to voter-approved investments in state land acquisitions designed to conserve and expand public parks over the past two years. Thanks to Proposition 14, which passed in November 2023, $1 billion in state funds was unlocked for the acquisition of private land for new state parks. “It does seem like there’s a growing pushback to oppose federal land ownership for conservation purposes,” says Marcy, “and we think it is very unfortunate, because the refuge system is possibly the best way of protecting land and habitat for wildlife.”

In oncology we return, again and again, to first principles. The cell is our unit of life and of medicine. When a normal cell becomes malignant, it does not merely divide faster; it eats differently. It hoards glucose, reroutes amino acids, siphons lipids, and improvises when a pathway is blocked. We have learned to poison its DNA, to derail its signaling, to enlist T cells as sentinels.

We have been slower to ask a simpler question that sits at the cell’s kitchen table: What if we change what a tumor can eat?

For a century, metabolism was oncology’s prologue. In the 1920s, Otto Warburg observed that many cancer cells consume glucose voraciously and convert much of that glucose to lactate even when oxygen is plentiful, a seemingly wasteful choice that became a metabolic signature of malignancy. That insight eventually receded into a footnote while genetics took the stage. But tumors are not static genotypes; they are shape-shifters that adapt to therapy by rewiring their fuel lines.

Therefore, if we want longer and deeper responses, the clinic has to treat metabolism as a first-class target. That means moving from one-size-fits-all “cancer diets” that tell nearly every patient to cut “sugar,” avoid white bread and pasta, drink green juices, or adopt alkaline regimens, regardless of tumor type, treatment, or physiology. Instead, oncologists should move to tumor-informed metabolism: interventions matched to the biology of a patient’s tumor, to the drug it is receiving, and to the body in which both reside.

Consider a woman in her 50s with hormone receptor-positive, HER2-negative breast cancer whose tumor carries a PIK3CA mutation. She receives a PI3K inhibitor alongside endocrine therapy. At first, the drug seems to hold; the scans steady, the markers fall. Then, over months, the cancer advances again. Blood work shows the clue: glucose and insulin levels, driven high by the drug’s effect on insulin signaling, have opened a back door for the tumor. The escape is not written in her genome; it is metabolically improvised.

So alongside the drug, she is given a dietary plan that trades sweetened drinks, desserts, and refined starches for slow-digesting carbohydrates, lipids, and proteins, crafted to blunt those insulin spikes, a protocol timed around dosing, calibrated to her physiology, monitored with real-time metabolic biomarkers. The tumor’s escape hatch narrows; the response deepens; the remission lasts longer. What made the difference was not drug alone or diet alone, but the braid of the two into a single therapy.

Metabolism is where ecology meets oncology. A tumor shares and competes for nutrients with its microenvironment. It burns different fuels in the liver than in the lungs. It shifts when a PI3K inhibitor raises insulin, and it shifts again if hyperglycemia follows steroids. Asparagine is dispensable for some cells, essential for acute lymphoblastic leukemia, which is why depleting it works. Serine and glycine can become growth linchpins in certain breast and colorectal cancers. Methionine restriction alters one-carbon flux in ways that make some tumors more susceptible to therapy. None of this is folklore. It is cell biology in the clinic.

Tumor-informed metabolism treats food as information. For a patient receiving a PI3K-pathway inhibitor, this might mean flattening post-meal glucose and insulin peaks. For a colorectal tumor that depends on particular amino acids, it might mean restricting those substrates during a course of chemotherapy or radiation. For a patient wasting away on treatment, it might mean adding calories and protein precisely because loss of weight and muscle would blunt the very therapy we hope will work. It begins with what the tumor uses, where it lives, which drug is acting upon it, and how the host responds. It is time-bound and measurable. It is designed to make a pharmacologic mechanism work better, not to replace it. It is delivered as precisely as a medication, with safeguards for weight, strength, and metabolic health.

In my work as a co-founder of Faeth Therapeutics, my colleagues and I build such regimens prospectively, pairing diets with PI3K/AKT/mTOR inhibitors in endometrial cancer, amino acid-restricted diets in rectal cancer, and scripting each plan around a specific mechanism and treatment window. Our intention, however, is less to advance a single company than to suggest a new template for how oncology might use food as a co-therapeutic instrument. I would welcome more companies designing similarly rigorous nutrition–drug regimens and submitting them to randomized trials, and I believe sponsors and regulators will eventually have to treat diet as a prespecified element of the protocol rather than an unmeasured backdrop.

The field is still in its infancy. There are encouraging signals across model systems in which pathway-directed drugs, such as PI3K inhibitors or chemotherapy/radiotherapy, have been combined with insulin-lowering or amino acid-modifying diets, but there are also failures when diets are generic, prolonged, or divorced from drug mechanism. Many patients lose weight during chemotherapy; some have diabetes; others fast zealously and end up weaker. Tumor-informed metabolism is an antidote to both nihilism and zeal. It treats nutrition as a targeted adjuvant rather than a belief system.

What will it take to make this part of standard care? The studies must be prospective, controlled, and anchored to a drug’s mechanism. Endpoints must be objective: response rates, survival gains, dose intensity preserved, and toxicity reduced. An intervention that shifts these curves deserves to be integrated into routine practice.

But evidence alone is not enough. We will need clinical structures that can hold and act on that evidence.

First, we will need multimodal regimens in pathways such as PI3K that shut down signaling without collapsing the immune response, avoiding the brittleness of single-node inhibitors and the collateral damage of indiscriminate blockade.

Second, we will need precision nutrition, not as lifestyle advice but as therapy: food scripted to complement a drug’s mechanism and to close the metabolic escapes the drug itself can provoke.

Third, we will need what might be called a metabolic operating system, a computational model of metabolism that lets us predict flux, anticipate resistance, and explore combinations in silico before they are carried into patients.

Without the unity of drug, precision nutrition, and model, tumor-informed metabolism remains a hypothesis. With it, medicine begins to see metabolism as a stratum of biology as fundamental as DNA or protein, but more immediate, revealing a cell’s state in seconds rather than years. “Feed the patient, starve the tumor” is not a slogan but a clinical directive, to be written with the same specificity as a chemotherapy order: macronutrient and micronutrient targets, timing, and contraindications.

There will be skepticism. Some will argue that metabolism is too plastic to trap, or that its contribution will be marginal. But oncology has always been built on combinations in which agents acting through different mechanisms, together, produce results greater than the sum of their parts: targeted drugs layered on chemotherapy, immunotherapies paired with radiation, and supportive drugs that preserve dose intensity and keep patients on treatment. If a tumor-informed plan buys three more cycles of a drug before resistance, that is not incidental to the person living those weeks.

Others will raise concerns about equity. They are right. If metabolism becomes a precision tool, it must be delivered as one: covered, accessible, adapted to diverse kitchens and cultures, not relegated to concierge care.

The deeper reason to do this is not tactical but philosophical. If the cell is the unit of life, then metabolism is the first verb in its sentence. We already intervene at the genome and the immunome. We should not ignore the part that feeds both. The clinic is where this becomes more than an idea. It becomes a plan the patient can taste, and a plan the tumor cannot.

Cancer medicine has always advanced by expanding what counts as therapy. We once thought cures would come only from sharper scalpels and stronger poisons. Then we learned to listen to T cells. Now we must listen to the hungers and handicaps of malignant cells, and use them. The next generation of combination therapy will not be drug plus drug alone. It will be drug plus metabolism, food braided with pharmacology, so that a tumor cannot simply sidestep us on a different substrate.

We will still sequence tumors. We will still give the best drugs we have. We will still sit with our patients on the hard days. But we can also do something elemental that does not subtract from strength or dignity. We can feed the person and starve the cancer, on purpose. That is an old idea made new by the precision of our time.

Siddhartha Mukherjee, M.D., D.Phil., is a physician, researcher, and author. A new edition of his Pulitzer Prize-winning book “The Emperor of All Maladies” is now available with four new chapters. He has co-founded several biotechnology and health care companies focused on developing novel cancer treatments, including Faeth Therapeutics and Manas AI. He also serves as associate professor of medicine at Columbia University and as an oncologist at the university’s medical center.