Given that ANGPTL3 is already a therapeutic target of dyslipidemia, it is reasonable to consider as future directions for questions including whether such regulation also applies to primary myeloid cells in the liver and whether it contributes to liver homeostasis under physiological or pathological settings in both mouse models and patients with hypertriglyceridemia and associated cardiovascular diseases. The gene discussed is ANGPTL3; the disease is cardiovascular disorder.