Furthermore, tailored exosomes with amplification of the miR-17-92 cluster facilitated neurogenesis, oligodendrogenesis, and axonal outgrowth via the PTEN/Akt/mTOR and GSK-3β pathways, which were previously shown to be key mechanisms in stroke recovery [13,14,21], and those with miR-133b increased neurite remodeling and synaptogenesis by regulating RABEPK, according to the studies of Xin et al. [20,44]. The gene discussed is RABEPK; the disease is stroke disorder.