LY86, also known as MD-1, can form a complex with RP105 to block the TLR4/MD-2 complex and, thus, attenuate inflammation via the NF-KB signaling pathway.[31] Therefore, an RP105 deficiency can lead to a slower progression of early atherosclerotic plaques.[32] Divanovic et al showed that RP105 can suppress TLR4 signaling only when MD-1 is fully present.[33] Therefore, the detailed mechanism by which the specific RP105/MD-1 complex leads to atherosclerosis needs to be further elucidated. The gene discussed is TLR4; the disease is atherosclerosis.