Notably, PD‐L1 could control inflammation after ischemic stroke[28] and significantly attenuate neurological deficits, ameliorate the inflammatory environment, and enhance the blood–brain barrier integrity in mice with intracerebral hemorrhage, by repressing the mammalian target of rapamycin pathway.[28, 29] Therefore, we genetically engineered MSCs overexpressing HGF and PD‐L1 to improve homing to target sites, modulate immunoreactions, and repair damaged tissues. The gene discussed is HGF; the disease is ischemic stroke.