As cardiac insulin signaling converges in translocation of GLUT4 receptor to the cardiomyocyte plasma membrane, and its disturbance is a key etiologic factor in diabetic cardiomyopathy,291 it is worthwhile to reiterate here the notion that FTO protects the murine heart from pressure-overload-induced dysfunction via Akt-mediated GLUT4 upregulation.175. Here, FTO is linked to diabetic cardiomyopathy.