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. This evidence concerns the gene CD28 and type 2 diabetes mellitus.