FOXM1 and glioblastoma: Therefore, ZNF217 depletion leads to impaired hypoxia‐induced consistent enrichment of BCSCs with ALKBH5 deficiency.74 In terms of glioblastoma, inactivated ALKBH5 inhibited the proliferation and tumorigenesis of GSCs and impaired GSCs self‐renewal.75 It is widely accepted that FOXM1 plays a pivotal role in regulating GSCs proliferation and self‐renewal.76, 77 ALKBH5 was found to demethylate FOXM1 nascent transcripts and promote FOXM1 expression, whereas long non‐coding RNA antisense of FOXM1 further promoted the interaction of FOXM1 nascent transcripts with ALKBH5.