It was recently described that the infiltration of T cells into the tumor endothelial barrier was mediated by the death mediator Fas ligand (FasL/CD95L) in the tumor vasculature of human and mouse solid tumors [169] and it was demonstrated that tumor-derived VEGF-A, IL-10 and prostaglandin E (PGE) cooperatively induced FasL expression in endothelial cells, allowing them to kill effector CD8+ T cells but not Treg cells, which express higher levels of c-FLIP. The gene discussed is IL10; the disease is neoplasm.