Blockade of this symbiosis by genetic depletion of TFPI2 in GSCs or pharmacologic inhibition of the TFPI2 receptor CD51 and its downstream STAT6 in microglia activates antitumor immunity and enhances the therapeutic efficiency of anti-PD-1 therapy in animal models of GBM tumors [223]. This evidence concerns the gene TFPI2 and glioblastoma.