Mutations in LDLR account for ∼85% of FH cases with the remainder caused by either loss-of-function mutations in the LDLR’s ligand Apolipoprotein B (APOB) (∼5–10%) or by gain-of-function mutations in Proprotein Convertase Subtilisin/Kexin type 9 (PCSK9) (∼2%) (Nordestgaard et al., 2013; Zubielienė et al., 2022). The gene discussed is APOB; the disease is familial hyperaldosteronism.