While hypertriglyceridemia is not viewed to be as linearly related to ASCVD risk as LDL-C, recent guidance has confirmed that the persistence of at least moderate (150–499 mg/dL) fasting hypertriglyceridemia is an important modifiable risk factor worthy of consideration for genetic predisposition (e.g., LPL [the product of which is lipoprotein lipase], APOC3, or ANGPTL3 variants [76]), secondary causes (e.g., uncontrolled DM, certain drugs), intensive therapeutic lifestyle changes, and, if necessary, pharmacologic treatment [77]. This evidence concerns the gene LPL and hypertriglyceridemia.