GS is an autosomal recessive tubulopathy associated with hypokalemia, metabolic alkalosis, hypomagnesemia, and hypocalciuria, resulting from mutations in the SLC12A3 gene encoding the thiazide-sensitive sodium−chloride cotransporter localized to the distal convoluted tubule [1,2]. This evidence concerns the gene SLC12A3 and familial primary hypomagnesemia.