HMGB1, on the other hand, activates the NF-κB pathway in Mφ via TLR4/RAGE signaling, promoting the secretion of chemokines such as CXCL9/CXCL10 and recruitment of effector T cells into the tumor microenvironment, while inhibiting Mφ polarization towards the M2 phenotype (20, 23). This evidence concerns the gene CXCL9 and neoplasm.