It is thought to affect tumor growth by two principal mechanisms: 1) through inhibition of mitochondrial oxidative phosphorylation, which activates AMPK thereby resulting in mTORC1 pathway inhibition, and 2) through decreased serum glucose, which inhibits IGF-R expression, thereby preventing downstream mTORC1 pathway activation in insulin-responsive cancers [44–50]. The gene discussed is INS; the disease is neoplasm.