Critically, FACS analysis of cell death using propidium iodide (PI) staining revealed that the cell death induced by PFKFB4 silencing was also significantly decreased when FBXO28 was silenced simultaneously (Fig. 6B, C), indicating that FBXO28 is indeed required for the degradation of HIF-1 α and subsequent cell death in GSCs upon silencing of PFKFB4. These results emphasize the novel role of PFKFB4 to protect HIF-1α from the SCF complex, enabling the expression of HIF-1α target genes and survival in glioblastoma stem-like cells (Fig. 6D). The gene discussed is KITLG; the disease is glioblastoma.