For example, canagliflozin inhibits mitochondrial complex I, activates AMPK via increased adenosine monophosphate:adenosine triphosphate ratio, and subsequently suppresses mTOR-driven lipid synthesis and proliferation in cancer cells. Dapagliflozin can reduce oxidative stress via AMPK-SIRT1 signaling and diminish proinflammatory pathways. By lowering systemic inflammation and oxidative stress, SGLT2 inhibitors may further counteract the tumor-promoting microenvironment that can accompany diabetes and ADT. This evidence concerns the gene MTOR and diabetes mellitus.