Mechanistically, when systemic bacterial infection occurred, ALKBH5 enhanced the expression of pro-neutrophil-migration molecules, such as CXCR2, and promoted the recruitment of neutrophils to the infection area to remove bacteria [78], indicating that ALKBH5 might serve as a key molecule involved in regulating the production of emergency granulocytes. This evidence concerns the gene ALKBH5 and bacterial infectious disease.