Having demonstrated that dapagliflozin slows tumor growth in two mouse models of obesity-associated cancer and that reversal of hyperinsulinemia is necessary for the in vivo tumor-suppressive effect of this SGLT2 inhibitor, we then examined a second insulin-lowering agent, CRMP, which works by an entirely independent mechanism: insulin sensitization [34], rather than calorie loss through glycosuria. The gene discussed is SLC5A2; the disease is hyperinsulinism.