Animal models of diabetes and high fat-induced obesity commonly demonstrate pathologies leading to elevations in serum levels of cTnI and cTnT including inflammation with IL-6 and tumor necrosis factor alpha (TNF-α), and inefficient generation of ATP resulting in increased ROS production, reduced contractility, ischemia, and increased demand ischemia [21,22]. The gene discussed is TNNT2; the disease is diabetes mellitus.