LDLR and familial hyperaldosteronism: Growing evidence showed that most FH are the result of heterozygous pathogenic variants in three different genes that encode key proteins involved in the endocytic and recycling pathways, such as the LDL receptor (LDLR), apolipoprotein B (APOB) and proprotein convertase subtilisin kexin 9 (PCSK9)3,4.