In 8/20 cases (40%), we could identify a variant that led to an ethio-pathogenical diagnosis of FH: four patients had heterozygous pathogenic or likely pathogenic variants on the LDLR gene (type 1 familial hypercholesterolemia), two patients had variants of unknown significance on the PCSK9 gene (type 3 familial hypercholesterolemia) and two patients had heterozygous mutations on the APOB gene (type 2 familial hypercholesterolemia). Here, LDLR is linked to familial hyperaldosteronism.