In agreement with this notion, Murase et al. reported that the inhibition of LPL caused hypertriglyceridemia in humans [35], and Berbee et al. reported that human APOC1 transgenic mice, who had a down-regulated LPL, showed hypertriglyceridemia and hypercholesterolemia [36]. The gene discussed is APOC1; the disease is familial hypercholesterolemia.