Using mice with site-directed mutagenesis for the TRAF6 or TRAF2/3/5 binding site on the CD40 intracellular tail, we demonstrated that CD40-TRAF6 interactions, and not CD40-TRAF2/3/5 interactions, promote the development of atherosclerosis and neointima formation [26, 27]. The gene discussed is TRAF6; the disease is atherosclerosis.