Although functional loss of SRs can result in hypercholesterolemia, which leads to atherosclerosis and heart disease, it has been shown that when the SR-B2 is exposed to modified LDL, it interacts with TLR4 and TLR6, resulting in NF-κB activation and contributing to the inflammatory response associated with atherosclerosis and promoting necrotic lesions of plaques (163, 164). This evidence concerns the gene TLR4 and atherosclerosis.