In addition to the increased expression of immunosuppressive molecules (e.g., FasL) and cytokines (e.g., IL-10 and TGF-β), tumor cells can directly escape T-cell recognition by downregulating MHC class I, by disabling other components of the antigen-processing machinery, and by upregulating surface ligands including PD-L1 and other ligands to inhibitory T-cell receptors, which mediate T-cell anergy (or exhaustion). Here, CD274 is linked to neoplasm.