In line with this study, research led by Joyce et al.69demonstrated that the CSF‐1R inhibitor PLX3397 (chemically distinct from BLZ945) also induces the repolarization of TAMs from an M2‐like state, the mechanism that restores the sensitivity of glioma cells to tyrosine kinase inhibitors in preclinical glioblastoma model. The gene discussed is CSF1R; the disease is glioblastoma.