In prostate cancer studies, canagliflozin showed inhibition of the activity of mitochondrial complex I, leading to the activation of AMPK and followed by the inhibition of mechanistic target of rapamycin complex 1 (mTORC1) and hypoxia-inducible factor 1-alpha (HIF-1α) pathways. The gene discussed is HIF1A; the disease is Familial prostate cancer.