In addition, over-expression of TLRs and other PRRs on the surface of phagocytic cells, or activation of endothelial cells and expression of adhesion molecules, such as ICAM1 or e-Selectin, are also signals known to promote efficient localization of phagocytes to the site of infection/tissue damage [39], [54], [55]. The gene discussed is SELE; the disease is infection.