Mustroph et al. (27) investigated the direct metabolic effects of SGLT2 inhibitors on cardiomyocytes and demonstrated that when isolated resting cardiomyocytes obtained from human end-stage heart failure transplanted hearts or transverse aortic constriction (TAC)-induced heart failure mouse hearts were treated with 1 μM of empagliflozin for 24 h in the presence of albumin, the expression of the glucose transporter protein GLUT1 increased. The gene discussed is SLC2A1; the disease is heart failure.