LDLR and familial hyperaldosteronism: Surprisingly, only few studies pertaining to the association of ER-stress with the molecular pathology of FH have been reported (Jørgensen et al., 2000; Sørensen et al., 2006; Kizhakkedath et al., 2019) in contrast to the fact that around 50% of LDLR mutations implicated in FH are class II mutants that are retained in ER due to misfolding.