Actually, phosphorylated STAT1 and STAT3 dimer in tumor cytosol can bind to the PD-L1 promoter to induce PD-L1 expression [42] while inhibition of STAT3 activity by STATTIC mitigates the CXCR3 activation-induced PD-L1 expression in tumor cells [21]. This evidence concerns the gene STAT3 and neoplasm.