GS is an autosomal recessive hereditary disorder characterized by hypokalemic metabolic alkalosis, hypomagnesemia, and hypocalciuria,[2] due to inactivating mutations in the solute carrier family 12, member 3 (SLC12A3) gene that encodes the thiazide-sensitive Na-Cl cotransporter.[3] GS was previously considered as a rare disease, with a reported incidence of approximately 1/50,000. Here, SLC23A1 is linked to familial primary hypomagnesemia.