Finally, we considered the fact that ApoC2 is a critical activator of LPL activity as shown by the fact that ApoC2 deficiency results in severe hypertriglyceridemia (23, 24, 25, 26, 27) and wondered what the effects of ANGPTL4/8-mediated plasmin generation might be on ApoC2-mediated stimulation of LPL activity. The gene discussed is LPL; the disease is hypertriglyceridemia.