NK cells have been originally designated for their considerable capacity of killing tumor cells, and the process and mechanism mediating their effect mainly includes ADCC and “missing-self” regulation; the latter one refers to the process that NK cells are normally repressed via binding with MHC I molecules [147], while cancer cells’ evolution trend towards downregulating their MHC I expression could reactivate NK cells to exert their effector function and supplement the immune evasion from CD8+ T cells [148]. Here, CD8A is linked to neoplasm.