Studies have shown that patients with ischemic cardiomyopathy display increased kinase activity of TNNI3K which may promote oxidative stress via impaired mitochondrial function and cardiomyocyte death, whereas inhibition of TNNI3K had protective effects and reduced adverse remodeling in the ischemic heart [7]. The gene discussed is TNNI3K; the disease is ischemic cardiomyopathy.