It has long been recognized that DM and HF are conditions characterized by a nutrient surplus, which leads to the inhibition of the nutrient deprivation sirtuin-1 (SIRT1)/HIF/5′ adenosine monophosphate-activated protein kinase (AMPK) pathway and the stimulation of the Akt/mammalian target of rapamycin complex 1 (mTORC1) pathway, resulting in increased endoplasmic reticulum stress, oxidative stress, inflammation, and apoptosis (Figure 1). The gene discussed is SIRT1; the disease is diabetes mellitus.