The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
what if the drug was causing diabetes separately from the tumor given to normal people that the drug would cause diabetes in some people worse than others and that diabetic phenotype a diabetic state the hyperinsulinemic state was being used or exploited by the tumor to essentially become resistant to the drug
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that's basically in animal models that happens to be true so we showed it using formal systems and formal methods that this insulin amia is a consequence of the drug has nothing to do with the tumour has nothing to do with anything else if you give the drug the drug goes into the liver and the pancreas and causes a sort of a pre-diabetic State that's often worsened that if you're already in a pre-diabetic State this hyperinsulinemia is used then by the tumor to become resistant even while the drug is present it becomes a pathway by which the tumor becomes resistant
what happens is that the body mounts an insulin emic response to the drug that insulin emic response goes to the cancer and starts feeding the cancer and then the cancer becomes resistant so you essentially undo all the good that you've done with the drug by cutting off your own limb because of this entry circuit
But that's the one that's going to need the most management of the hyperglycemia and the hyperinsulinemia.