Knockout of HIF1α and HIF2α in CD133−CD15− GBM cells (Fig. S15C, Fig. S16A) significantly reduced aggregation formation (Fig. 6C, Fig. S16B) and stemness marker expression, including CD133, CD15, Nestin, Sox2, and Klf4, particularly under simultaneous knockout of HIF1α and HIF2α after TMZ treatment (Fig. 6B, Fig. S16A). The gene discussed is HIF1A; the disease is glioblastoma.