CXCL8 and neoplasm: A number of researchers have proposed that hypoxia-induced ALKBH5 stabilizes transcripts and promotes relocalization of the transcriptional repressor, SFPQ, from the CXCL8 promoter to paraspeckles by eliminating the deposition of m6A-methylated lncRNA NEAT1, ultimately stimulating tumor macrophage recruitment and tumor immune escape through upregulation of CXCL8/IL8 in glioblastoma [32].