Abstract: N⁶-methyladenosine (m⁶A) methyltransferases encompass "Writers" "Erasers" and "Readers" proteins, which influence the immune response and neurorepair process in stroke by modulating the M1/M2 polarization state of microglia, cytokine secretion, and neurorepair factor expression. m⁶A methylation exacerbates inflammatory responses in the acute phase by promoting pro-inflammatory factor expression and M1 polarization, while in the recovery phase, it facilitates tissue repair and neuroregeneration by increasing anti-inflammatory factor expression and M2 polarization. This paper reviewed the molecular mechanisms of m⁶A methylation-related enzymes and their bidirectional roles in the functional regulation of microglia, and evaluated the feasibility of m⁶A methylation as a potential therapeutic target for stroke, aiming to provide new research perspectives and therapeutic strategies for immune regulation and neurorepair in ischemic stroke.