FH has long been considered a highly penetrant disease, with rarely anyone having a plasma LDL cholesterol (LDL-C) concentration below the 95th percentile of the general population (Miserez and Keller, 1995), however a recent finding that pathogenic or likely pathogenic FH mutations were present even in subjects with LDL<3.3 mmol/L contributing to 27% of total mutation-positive subjects in a large study suggests large heterogeneity in the clinical expression of monogenic FH (Khera et al., 2016; Sniderman et al., 2022). Here, FH is linked to familial hyperaldosteronism.