Our findings address these challenges by establishing that (1) TAK901 reduces the viability, self-renewal, migration, invasion, and induces apoptosis and cell cycle arrest in both GBM and GSC cells; (2) TAK901 suppresses GBM growth in orthotopic mouse models; (3) TAK901 suppresses the expression of lipid metabolism pathway-related genes and reduces intracellular lipid droplets in GBM; and (4) TAK901 inhibits SREBP1 expression in GBM cells, whose overexpression attenuates the TAK901-mediated suppression of cell viability and apoptosis. The gene discussed is SREBF1; the disease is glioblastoma.