In agreement with this hypothesis, the prevalence of FH in a German registry (11) was 1.2% (2/166 patients), all with clinical FH-II (but the diagnosis was based only on familial history of PA, without demonstration of pathogenic variants in the CLCN2 gene), and in an Australian study 0.36% for FH-I and 2.8% for FH-II (also based only on familial history of PA, without demonstration of pathogenic variants in the CLCN2 gene) (44). Here, CLCN2 is linked to familial hyperaldosteronism.