It illustrates that FH patients of similar age, sex, and risk profile, originating from France and French Canada, sharing well-documented IBD pathogenic LDLR variants having evolved in different geographic, cultural, and socio-economic environments for hundreds of years, may differ in terms of cholesterol levels (Figure 1), highlighting the importance of better understanding the interplay between genetic and environmental modulators of FH expression. The gene discussed is LDLR; the disease is familial hyperaldosteronism.