The results from LPL-deficient mice and mice with induced LPL-deficiency, which do not readily develop atherosclerosis or exhibit impaired lesion regression, appear to be consistent with studies on homozygous LPL-deficient human subjects, whereof very few develop premature atherosclerosis (92–94), supporting the hypothesis that homozygous LPL deficiency causes accumulation of large TRLs which cannot effectively promote atherosclerosis. The gene discussed is LPL; the disease is atherosclerosis.