One of the mechanisms of hyper‐reabsorption of glucose is an increased expression of sodium/glucose cotransporter‐2 (SGLT2) in patients with T2D and diabetic nephropathy.2, 3 Increased SGLT2 induces increased proximal tubular reabsorption of, not only glucose, but also sodium, both of which are SGLT2 substrates. Here, SLC5A2 is linked to diabetic kidney disease.