GS is the consequence of a biallelic mutation affecting the SLC12A3 gene causing the inactivation of thiazide‐sensitive sodium chloride cotransporter (NCC) in the DCT,2 thus resulting in a salt‐wasting tubulopathy with volume contraction, hyper‐reninism, and hyper‐aldosteronism. This evidence concerns the gene SLC12A3 and Gerstmann syndrome.