NAFLD development is partly driven by glucotoxicity.4-6 Clinical trials of sodium-glucose cotransporter-2 inhibitors (SGLT-2i), which inhibit renal tubular glucose absorption, demonstrate that in patients with T2D and NAFLD, SGLT-2i improves liver enzymes and reduces liver fat.7-9 SGLT-1 is a potent mediator of intestinal glucose absorption that contributes to NAFLD through increased glucose flux to the liver. Here, SLC5A1 is linked to metabolic dysfunction-associated steatotic liver disease.