Similarly, STAT1 has been suggested to act as a point of convergence for the cross-talk between the pro-atherogenic TLR4, IFN-γ, and IL-6 activated pathways in immune as well as vascular cells, amplifying pro-inflammatory signals, increasing endothelial cell adhesion, and possibly promoting the development of atherosclerosis [41]. This evidence concerns the gene TLR4 and atherosclerosis.