Targeting FOXM1 reduced AXL and eEF2K expression, suggesting that FOXM1-targted therapies may offer multitargeting potential due to suppressing AXL/eEF2K signaling, leading to the inhibition of cell proliferation, cell migration–invasion, and spheroid formation ability and causing apoptosis and ferroptosis induction in GBM cells (Figure 8). This evidence concerns the gene FOXM1 and glioblastoma.