Such findings suggest that in a tumor environment, IFN-γ can through its IFNR1/2 receptors activate the JAK/STAT3 signaling to directly induce PD-L1 expression and enhance CXCL9 expression, which indirectly through its CXCR3 activates the STAT3 and Akt signaling to up-regulate PD-L1 expression in tumor cells [21, 38, 41]. This evidence concerns the gene AKT1 and neoplasm.