Different mechanisms have been proposed to explain the cardioprotective effects of SGLT2 inhibitors, such as an increase in diuresis/natriuresis, autophagy, lysosomal degradation, circulating pro-vascular progenitor cells, erythropoiesis and erythropoietin levels; decrease in blood pressure, oxidative stress, hyperuricemia, inflammation, myocardial fibrosis, and epicardial fat mass; improvement in energy metabolism and vascular function; inhibition of sympathetic nervous system, Na+/H+-exchanger, and SGLT1; and prevention of ischemia/reperfusion injury [12,56,57]. This evidence concerns the gene SLC5A1 and hyperuricemia.