Suppressing the proliferation of cells (anti-proliferative effect) in a dose-dependent way (5–50 μM) through EGF-mediated FAK/AKT pathwayInhibiting the cell viability (5–50 μM)Restraining the cell survival of glioblastoma cells in a dose and time-dependent way (10, 20, 30 μM) for 24, 48, or 72 hReduction in the phosphorylation of FAK and AKT in glioblastoma cells (10 μM of harmine)Inhibiting the migration and promotes apoptosis in GBM and affects the expression of related proteinsInhibiting the migration of U251-MG cells. This evidence concerns the gene EGF and glioblastoma.