Although ApoC3 inhibition has been applied for the treatment of HTG in different clinical trials, however, unlike ANGPTL3, an inhibitory regulator of LPL activity was recently accepted as a potential therapeutic target for both HTG and hypercholesterolemia, whether targeting ApoC3 has beneficial effects on refractory hypercholesterolemia and consequential outcome of atherogenesis in the context of FH due to dysfunctional LDLR is still elusive. The gene discussed is LDLR; the disease is familial hyperaldosteronism.