As we found that the MEK/Erk signaling was most critical in constitutive expression PD-L1 and the down-regulation of NKG2D ligands in cisplatin-resistant cells, we next tested whether the addition of the MEK/Erk inhibitor to the primary NK/tumor cell co-culture might enhance the PD-L1 Ab effect on increasing the susceptibility of cisplatin-resistant cells to NK cell action. The gene discussed is KLRK1; the disease is neoplasm.