Recently, Pyonteck et al. (2013), demonstrated that in a mouse model of glioblastoma, when they used a CSF-1 inhibitor to target tumor associated macrophages (TAM) surprisingly, cells were re-educated to change the tumor-induced M2 phenotype, in which arginase I was protumorigenic, toward a M1 anti-tumor phenotype maintained by GM-CSF and IFN-γ secreted by the tumor with the potential to actively kill glioma cells. This evidence concerns the gene CSF2 and neoplasm.