Hamzei et al. found that the intracerebral injection of miR-124 suppressed development of inflammation by skewing the microglia into the M2 anti-inflammation phenotype after ischemic stroke [13], which could release anti-inflammatory factors such as interleukin (IL)-10, IL-4, and IL-13, transforming growth factor β, and activating T regulatory cells [73], subsequently improving tissue repair and long-term neurological outcomes after ischemic stroke. Here, IL13 is linked to ischemic stroke.