In addition to these 2 proinflammatory factors, after CD40 ligation on macrophages and binding with CD40L on T cells, activated macrophages can synthesize and secrete matrix metalloproteinases, MIP-1, MCP-1, IL-8, TNF-α, IFN-γ, as well as tissue factor to affect thrombosis.[60] Recent research has shown that the application of small molecule inhibitors that block the interaction between CD40 and TRAF6 can preserve CD40-mediated immunity by allowing CD40-TRAF2/3/5 interactions to be used for the treatment of atherosclerosis.[61,62]. The gene discussed is CD40; the disease is atherosclerosis.