A more recent study revealed that CAFs directly contribute to the suppression of antitumor T cell responses by cross-presenting antigens complexed with major histocompatibility complex (MHC) I to antigen-specific CD8+ T cells, leading to antigen-specific upregulation of Fas/FasL and PD-1/PD-L2 on T cells and CAFs, respectively, which ultimately results in elimination of tumor-specific T cells and enhanced tumor viability [71]. The gene discussed is PDCD1LG2; the disease is neoplasm.