CD36 has been shown to contribute to inflammatory responses to various pathogens and to endogenous pathogenic components such as β-amyloid plaque and low-density lipoprotein complex through the receptor-mediated activation of mitogen-activated protein kinase (MAPK) and NF-κB signaling pathways, leading to high levels of inflammation and pathogenesis of diseases such as Alzheimer’s disease, atherosclerosis, diabetes, and infectious diseases [19], [20], [57], [58]. This evidence concerns the gene NFKB1 and atherosclerosis.