While its dysregulation has been implicated in the progression of various human malignancies, including enhanced invasion, migration, and metastasis [21,22,23], the role of FoxM1 in the context of cerebral ischemia, particularly as a potential mediator of hAEC-derived exosome effects, remains poorly understood and warrants focused mechanistic exploration. This evidence concerns the gene FOXM1 and Cerebral ischemia.