The novel and important findings of this study are that (1) the mechanisms regulating LDL-receptor mediated endocytosis are restored in genetically corrected FH iPSC and HLC, and (2) statin-mediated accumulation of misfolded LDLR did not induce ER stress in class II FH iPSC or HLC with ∼5% LDLR activity. This evidence concerns the gene LDLR and familial hyperaldosteronism.