Molecular diagnostics testing is recommended (but phenotypic diagnosis is sufficient to start therapy) and allows for genetic testing for mutations in genes responsible for FH: the most common are in the LDL-C receptor (LDLR), apolipoprotein B (apoB), proprotein convertase subtilisin kexin type 9 (PCSK9), and more rarely the LDLR adaptor protein (LDLRAP1) and apolipoprotein E (APOE) [1,5,6]. This evidence concerns the gene APOB and familial hyperaldosteronism.