Stroke remains a leading cause of death and disability worldwide.1 Despite decades of research, tissue-type plasminogen activator and endovascular devices are the only available treatment options.2 However, because of a narrow therapeutic time window and potential contraindications, only 3% to 5% of stroke patients are able to benefit from these interventions.3 This highlights the need for a broader understanding of tissue injury mechanisms to develop more effective treatments. This evidence concerns the gene PLAT and stroke disorder.