A combination of these methods enabled us to define the distinct characteristics of both wild‐type and variant tPA (tenecteplase: TNK [T103N, N117Q, K296A, H297A, R298A, R299A]‐tPA), the latter of which is shown to be associated with better reperfusion and clinical improvement as a thrombolytic drug for patients with stroke compared to wild‐type tPA (alteplase) 7 and with safe and feasible agents for minor stroke with intracranial occlusion 8. The gene discussed is PLAT; the disease is stroke disorder.