Random thoughts: Obesity may be a systemic version of the tumor microenvironment. Could restoring NK metabolic fitness let a lower, tolerable systemic dose of IL-15 agonist actually work? Obesity paradox” in immunotherapy. Obese patients often respond better to checkpoint inhibitors, not worse. If obesity purely broke anti-tumor immunity, that shouldn’t happen. Glp1: What we do know: after stopping semaglutide, roughly two-thirds of lost weight comes back within a year. And the regain is disproportionately fat. So the plausible model is: •On drug: low insulin, low lipid overflow → myosteatosis doesn’t re-accumulate. Transmitter stays clean. •Off drug: fat returns first, muscle doesn’t. You can end up with a worse body composition than you started with. Which means the “cleaning” is rented, not owned — unless you built something while you had the window. That’s an argument for load, not for the drug.