CXCL8 and neoplasm: Dong et al. showed that ALKBH5 was responsible for m6A depletion on lncRNA NEAT1 in glioblastoma cells and increased transcript stability, allowing the transcriptional repressor SFPQ to relocate from the CXCL8 promotor to nuclear paraspeckle bodies, leading to upregulation of IL-8 in the tumor microenvironment and tumor-associated macrophage (TAM) recruitment.