Gitelman’s syndrome (GS), also known as, familial hypokalemia–hypomagnesemia, is a renal tubulopathy responsible for salt wasting resulting in, hypomagnesemia, hypocalciuria, and secondary activation of the renin–angiotensin–aldosterone system, responsible for the hypokalemia and metabolic alkalosis.1,2 GS is due to a rare, autosomal recessive gene mutation due to deletions, missense, nonsense, frame-shift, and splice-site mutation in the solute carrier family 12, member 3 (SLC12A3) gene. This evidence concerns the gene SLC12A3 and Gitelman syndrome.