AQP4 KO mice exhibited significant astrocyte swelling, increased infarct size, and severe CA1 neuronal loss, exacerbating brain damage 72 h post‐MCAO/R.[30] In addition, AQP4‐deficiency mice showed greater neutrophil infiltration and microglial activation than wild‐type mice at 24 and 72 h post‐MCAO/R.[31] The dual role of AQP4 in stroke progression is critical to understanding the variable effects of TGN‐020 in ischemia models. This evidence concerns the gene TG and stroke disorder.