These receptors may fine-tune the γδ T cell activation threshold, enhance γδ T cells to recognize tumor target, prompt γδ T cells to mediate an immediate immune reaction against tumor target, and release cytotoxic granules such as perforin and granzyme B. In cancer, the down-regulation of MHC-I may prompt ‘missing-self recognition’, which unlock the binding between MHC-I and inhibitory receptors on γδ T cells, making γδ T cells unhindered to attack tumor cells in a NK-like manner (6). Here, PRF1 is linked to neoplasm.