Despite increased lipolysis of TRLs by LPL and reduced TG in apoC-III-deficient mice [112], no difference in atherosclerosis burden was noticed in the apoC-III-deficient mice compared to the control on LDLR-deficient background [115], although humans with apoC-III loss-of-function mutations showed apparent cardio-protection in carriers compared to non-carriers, based on subclinical atherosclerosis findings measured by calcium score [116]. This evidence concerns the gene LDLR and atherosclerosis.