Conversely, TAMs have been shown to drive glioblastoma cells to a MES‐like state in vivo through the STAT3 activation downstream of receptor tyrosine kinase AXL and oncostatin M receptor (OSMR), targeted by Amphiregulin (AREG), Heparin‐binding EGF‐like growth factor (HBEGF) and OSM ligands expressed on macrophages. Here, STAT3 is linked to glioblastoma.