Secondly, PZH attenuated the immune escape ability of CRC cells via inhibiting the IFNGR1-JAK1-STAT3-IRF1 signaling to down-regulate the level of PD-L1, which relieving the repression of CRC cells dependent PD-L1 inhibitory molecules on CD8+ T cells; these regenerated CD8+ T cells activated at the tumor site and exerted antitumor function. This evidence concerns the gene STAT3 and neoplasm.