Given the complexity and probable multiple redundancies built into signaling pathways that drive a tumor-associated macrophage M2 phenotype, it is unlikely that signal agent blockade of any particular function will be sufficient to alleviate immune suppression in the tumor microenvironment, although several options may hold potential, notably inhibition of STAT3 and wnt/β-catenin signaling. This evidence concerns the gene STAT3 and neoplasm.