In our previous study, inhibition of Semaphorin 3A in the subacute stage of stroke suppressed the activation of astrocytes and downregulated miR-30c-2-3p and miR-326-5p in astrocyte-derived exosomes, which were capable of enhancing axonal elongation in ischemic neurons by increasing prostaglandin D2 synthase [13]. The gene discussed is SEMA3A; the disease is stroke disorder.