GS is caused by a variety of mutations within the genes encoding SLC12A3 (thiazide-sensitive sodium chloride cotransporter (NCC): HNF1B (hepatocyte nuclear factor 1β), FXYD2 (sodium/potassium-transporting ATPase gamma chain—a member of the FXYD family of transmembrane proteins), KCNJ10 (ATP-sensitive inward rectifier potassium channel 10, a member of the inward rectifier-type potassium channel family) [16,36,37,38,39]. Here, KCNJ10 is linked to Gerstmann syndrome.