These include hypercalciuric hypomagnesaemias (secondary to mutations inCLCNKB (Bartter syndrome type 3),CLDN16,CLDN19,CASR); Gitelman-like hypomagnesaemias (secondary to mutations inSLC12A3 (Gitelman syndrome),BSND (Bartter syndrome type 4),KCNJ10,FXYD2,HNF1B,PCBD1); mitochondrial hypomagnesaemias; (mutations inSARS2,MT-TI and Kearns–Sayre syndrome) and other hypomagnesaemias (secondary to mutations inTRPM6,CNNM2,EGF,EGFR,KCNA1,FAM111A,ATP1A1)5. This evidence concerns the gene ATP1A1 and Bartter disease type 3.