LPL and atherosclerosis: The rare haplotype in vivo would result in the reduction of apolipoprotein AV synthesis, and thus there was less apolipoprotein AV that was available for incorporation into triglyceride-rich particles, with the consequence of less circulating apolipoprotein AV to promote the activation of lipoprotein lipase or to affect its receptor-mediated clearance, eventually developing atherosclerosis [10, 42].