Possibly evasive mechanisms include down-regulation of MHC Class I that prevents TE cells from engaging their tumor target [42], the recruitment of regulatory T cells that can directly and indirectly (modulation of cytokine environment) impairs TE function [43] and the up-regulation of checkpoint ligands such as PD-L1 that are known to engage PD-1 on TE cells and interfere with TCR signaling, impairing cytolytic function [44]. The gene discussed is CD274; the disease is neoplasm.