More recently, another study showed how the secretion of IL-33 from glioma cells and the presence of nuclear IL-33 within them initially act to recruit monocytic cells with an M1-like antitumorigenic phenotype from circulation and then, favor the reprogramming of the TAMs to a pro-tumorigenic M2-like phenotype that in turn fuels rapid glioma growth [81]. This evidence concerns the gene IL33 and central nervous system cancer.