They elegantly demonstrated, using transgenic expression of human LPL in ApoA5 knockout mice and ApoA5 overexpression in LPL deficient mice, that increased LPL activity normalized hypertriglyceridemia in ApoA5 knockout mice, while ApoA5 overexpression affected plasma TG levels only slightly when LPL activity was reduced (20). This evidence concerns the gene APOA5 and hypertriglyceridemia.