In addition, RuPOP co-acts with NK cells; in addition to directly damaging tumor cells, it can also trigger CaspasE3-dependent apoptosis by upregulating NKG2D and its multiple ligands, induce ROS production, and activate a variety of apoptosis-related receptors, such as tumor cells and tumor cells, so as to maximize the interaction between NK cells and tumor cells(as shown in Table 1). Here, KLRK1 is linked to neoplasm.