Finally, we verified the therapeutic mechanisms of PLX3397 via immunohistochemistry, and the results demonstrated that PLX3397 prominently reduced cell proliferation (Ki67 staining), increased apoptotic cell death/signaling (TUNEL staining, cleaved caspase-3), reduced GBM cell invasion (H&E staining, Vimentin) and CSF1R-downstream signaling pathway p-PI3K/p-AKT [45, 46] (Fig. 2I–P). Here, AKT1 is linked to glioblastoma.