Our results revealed that PD-L1/PD-1 signaling blockade could induce an elevation of NKG2D expression levels, and this increase might be a concomitant consequence with the release of multiple immune-promoting molecules, such as IFN-γ that we have shown to directly stimulate the levels of NKG2D on CIK cells, which is compatible with the previous study demonstrating that NKG2D molecule could be modulated by various cytokines and tumor-derived factors [45], and with clinical specimen analysis showing NKG2D expression positively correlated with IFN-γ level (Supplementary Figure S6). The gene discussed is PDCD1; the disease is neoplasm.