CLDN19 and familial primary hypomagnesemia with hypercalciuria and nephrocalcinosis: The orchestrated action of these organelles is key for cellular homeostasis and survival under pathological stress conditions [33] and may explain the variability of the clinical phenotype in FHHNC in which the endoplasmic reticulum (ER) is likely to be under high stress due to the reported retention of CLDN19 p.G20D mutant protein [5].