The ability of APOC3 to prevent LPL’s action could explain why in a very hypertriglyceridemic LDLR-deficient hamster model, APOC3-deficiency, despite lowering plasma triglycerides, resulted in increased atherosclerosis (51); it is possible that increased LPL-mediated hydrolysis of TRL triglycerides brought about by APOC3-deficiency might have resulted in increased atherogenic remnant formation. The gene discussed is LPL; the disease is atherosclerosis.