As reported, METTL3-mediated m6A modification respectively promoted acute kidney injury, acute lung injury and acute brain injury via promoting TAB3 expression in an IGF2BP2 dependent manner 12, activating ferroptosis by upregulating ACSL4 under histone acetylation 13, driving neuroinflammation and neurotoxicity through stabilizing Batf mRNA in microglia 14, indicating that targeted-METTL3 inhibition was a promising therapy in acute organ injury. This evidence concerns the gene METTL3 and brain injury.