This result is consistent with our study where increased activation of STAT3 by iMSC-sEV promoted angiogenesis and inactivation of STAT3 by stattic partially attenuated this effect, indicating a potential STAT3-involved mechanism in iMSC-sEV-induced pro-angiogenic ability after ischemic brain injury, while, a recent paper reported that inhibition of STAT3 by stattic improved blood brain barrier (BBB) integrity after stroke [64]. The gene discussed is STAT3; the disease is Stroke.