In diabetes, increased expression and activity of SGLT2, and fully activated SGLT1, account for almost 50 g of sodium, which may represent over 10% of the filtered sodium load, may be reabsorbed via SGLT‐dependent pathways.11 Although post meal urinary sodium excretion, in addition to urinary glucose excretion, was increased from baseline, both acutely and chronically, by administration of an SGLT2 inhibitor (SGLT2i),12 little is known about the association of sodium intake with the clinical effects of SGLT2is. Here, SLC5A2 is linked to diabetes mellitus.