KLF15 and Hepatic steatosis: While previous reports implicate a molecular mechanism involving KLFs and NRs in the context of, but not limited to, neuronal differentiation and ischemic stroke [44, 45], smooth muscle biology [46], prenatal lung differentiation [47, 48], hepatic steatosis [49], endometriosis [50], and browning of adipocytes [51], this report is the first demonstration that KLFs and NRs, in general, and KLF15 and PPARα, in particular, coordinate metabolic gene expression and function in the cardiomyocyte.