CAFs can disturb the anti-tumor activity of effector T cells by inducing the expression of immune checkpoint molecules, such as FAS/FASL and PD-1/PD-L1 or PD-L2, on their surface, followed by decreased CD8+ T cell frequency and activation and, in contrast, increased tumor cell viability (36, 37). The gene discussed is FASLG; the disease is neoplasm.