“Loss‐of‐function” mutations decrease LDL receptor degradation and patients with these mutations have low LDL‐C concentrations and appear to be protected from coronary heart disease.10 Conversely, “gain‐of‐function” mutations accelerate LDL receptor degradation and carriers of these mutations present with elevated LDL‐C levels and heightened cardiovascular risk.5 In these patients, the clinical features are similar to those observed in FH patients with LDL receptor mutations. The gene discussed is LDLR; the disease is familial hyperaldosteronism.