In apolipoprotein E (apoE) KO mice with hyperlipidemia-induced atherosclerosis, PCSK9 silencing inhibits the progression of plaque volume, the accumulation of macrophages in lesion areas, and the secretion of inflammatory cytokines, such as TNF-α and IL-1β, by macrophages, which is accompanied by limited intracellular activation of the TLR4/NF-κB pathway (32). This evidence concerns the gene APOE and atherosclerosis.