Given the potential neurovascular benefits of sEH inhibitors in preclinical stroke models and their safety profiles in humans24,25, our findings indicate that TrkB activation is involved in sEH blockade-mediated neuroprotection in acute ischemic stroke and open new possibilities for combination treatments with neuroprotectants and reperfusion by thrombolytic and/or endovascular thrombectomy treatments. The gene discussed is NTRK2; the disease is stroke disorder.