Sodium-glucose cotransporter-2 inhibitors (SGLT2Is) act as weak diuretics, inhibiting glucose and sodium reabsorption in the renal proximal tubules.1 They increase the risk of diabetic ketoacidosis, particularly euglycemic diabetic ketoacidosis, as reduced serum glucose promotes ketogenesis.2 While SGLT2Is show potential for managing refractory ascites in cirrhosis,3,4 safety data in advanced liver disease is limited.5,6 We report a case of nondiabetic ketoacidosis that occurred shortly after empagliflozin initiation in a patient with advanced alcoholic-associated liver disease. This evidence concerns the gene SLC5A2 and Cirrhosis.