Because human studies convincingly show that loss-of-function mutations in APOC3 are associated with lower TG levels and cardioprotection (121, 122, 171–174), APOC3 has recently emerged as a drug target for the treatment of hypertriglyceridemia and possibly the associated increase in CVD risk (18, 175–177). This evidence concerns the gene APOC3 and hypertriglyceridemia.