In this report we close the genetic gap by unraveling the prevalence of yet another founder mutation in LDLRAP1 that combined with the LDLR variants (p.C681*, p.H327fsX5, p.A391T, and p.I451T) accounts to 100% of the population prevalence of FH in Lebanon. The gene discussed is LDLR; the disease is familial hyperaldosteronism.