Within the first few hours after the onset of stroke, despite the return of blood flow with or without tissue plasminogen activator (tPA) or endovascular thrombolysis, ischemia–reperfusion injury and neuronal damage may result in multiple pathological events such as excitotoxicity, necrosis, oxidative stress, inflammation, apoptosis, platelet adhesion, and blood–brain barrier (BBB) disruption (Lin et al., 2016; Mayor and Tymianski, 2018; Andjelkovic et al., 2019). The gene discussed is PLAT; the disease is stroke disorder.