During neuroinflammation, T cell-specific ALKBH5 ablation has been shown to diminish neutrophil recruitment into the central nervous system of mice with experimental autoimmune encephalomyelitis by decreasing Cxcl2 mRNA stability in CD4+ T cells.16 Our findings in this study reveal previously unknown role of ALKBH5 and its m6A demethylation in neutrophil migration by endowing neutrophils with intrinsic ability to response to extrinsic chemokine signals and to migrate into infection sites. Here, ALKBH5 is linked to experimental autoimmune encephalomyelitis.