Under hypoxic conditions, the stability of LncNEAT1 is increased because its m6A modification is eliminated by ALKBH5, and the posttranscriptional repressor SFPQ is relocated from its position in the CXCL8 promoter to paraspeckles, ultimately upregulating CXCL8/IL8 and promoting glioblastoma multiforme (GBM) progression103. This evidence concerns the gene CXCL8 and glioblastoma.