Altogether, HTN-T2DM hearts might lead to reduced glycolysis and gluconeogenesis and decreased AMPK and fatty acid oxidation, which would induce significant damage to mitochondria (i.e., oxidative phosphorylation, PGC1α, MYC), increased inflammation (CD28, NFEL2), and adaptive cardioprotective responses including Rictor activation. The gene discussed is MYC; the disease is hypertensive disorder.