The current data suggest that any ‘new‐FH gene’ is likely to explain a smaller proportion of cases than either the APOE or PCSK9 loci (i.e., less than ∼1% of clinical FH individuals) since if such a common cause of FH were present it would have been already identified by the studies carried out to date. This evidence concerns the gene PCSK9 and familial hyperaldosteronism.