Based on our data, we suggest that [Fe‐S] cluster homeostasis may be imbalanced in renal tubular cells from FHHNC patients with a more severe renal phenotype contributing, therefore, to the aggravation of the high cellular stress already produced by the CLDN19 mutation. The gene discussed is CLDN19; the disease is familial primary hypomagnesemia with hypercalciuria and nephrocalcinosis.