These results indicate that irinotecan may suppress the host’s antitumor immune response via up-regulation of PD-L1 on tumor cells, regardless of the increase in antigen-presentation from tumor cells via up-regulation of MHC class I. Therefore, blockade of PD-L1 by the combination treatment may allow the intrinsic immune system to exploit the irinotecan-enhanced antigen stimulation. This evidence concerns the gene CD274 and neoplasm.