Additionally, in the CSF-1R inhibition therapy of GBM, Quail et al. found that the PI3K cascade can also be activated by TAM-derived insulin-like growth factors1 (IGF-1), as a result, promoting tumor cells to be resisted to BLZ945, a type of CSF-1R inhibitor, and the application of PI3K inhibitor (BKM120) could rescue the chemosensitivity of GBM in CSF-1R inhibition therapy [121]. Here, CSF1R is linked to neoplasm.