In fact, in non-diabetic preclinical models of nephropathies, dapagliflozin, a SGLT2 inhibitor, reduced proteinuria and podocyte damage [22], and empagliflozin, a SGLT2 inhibitor, improved renal function in obese Zucker rats [23], reduced renal dysfunction and fibrosis in unilateral ureteric obstruction [24], regulated the circadian rhythm of blood pressure in salt-treated obese rats [25], and finally prevented the development of renal fibrosis through an anti-inflammatory mechanism in Ang II-dependent hypertension [26]. The gene discussed is SLC5A2; the disease is renal fibrosis.