A recent study found that SGLT2 is expressed in the cardiomyocytes from patients with end-stage HF irrespective of their HF cause.42 Interestingly, SGLT2 is overexpressed in diabetic cardiomyocytes, suggesting that hyperglycaemia may act on cardiomyocytes, increasing SGLT2, and thus supporting the hypothesis of the effect of SGLT2 mediation on metabolic pathways in patients with HF.43–45 However, changes in cardiac and renal metabolism and energy use cannot fully explain the benefits of SGLT2i on patients with cardiorenal stress. This evidence concerns the gene SLC5A2 and hydrops fetalis.