MyD88-dependent signalling is associated with downstream activation of NF-kB and production of pro-inflammatory cytokines and chemokines.9 TRIF-dependent signalling is typically associated with IRF3 and production of type 1 IFN, as well as late phase NF-kB activation via TRAF6.9 While TLR3/TRIF-dependent signalling may have some protective effect against cardiovascular disease, TLR4/TRIF-dependent signalling is considered pro-atherogenic.10 Therefore, TLR4-specific antagonists of TRIF signalling are also of great interest for treatment of these diseases. This evidence concerns the gene TICAM1 and cardiovascular disorder.