Anti-cancer therapy using multikinase inhibitors, e.g., sorafenib and sunitinib, were not only effective in reducing tumor growth, but also inhibited STAT3 expression in MΦs, whereby IL-10 secretion was blocked and IL-12 was induced, thus suggesting an immune activating TAM phenotype [107] Moreover, treatment of glioblastoma patients with WP1066 inhibited STAT3 activation and induced the expression of pro-inflammatory cytokines in MΦs, whereby T cells were activated, finally reducing immunetolerance [108]. Here, STAT3 is linked to neoplasm.