In summary, our results show that the upregulation of BRMS1 in microglia may activate the PI3K/AKT signaling pathway in GBM through SPP1/CD44-mediated interactions, regulate the expression of apoptosis-related proteins Bax, Bcl2, and cleaved-caspase 3, thereby inhibiting the apoptosis of GBM cells. Here, BCL2 is linked to glioblastoma.