Currently, Light et al. demonstrated that INa,L is one of the major targets for the antiarrhythmic effect of SGLT2i, increasing in cardiomyocytes from mice with HF induced by transverse aortic coarctation and in cardiac Nav1.5 sodium channels containing the long QT syndrome 3 mutations, and SGLT2i (dapagliflozin, empagliflozin and canagliflozin) inhibited INa,L in a concentration-dependent manner, with little inhibitory effect on INa,P. This evidence concerns the gene SCN5A and hydrops fetalis.