Additionally, aCL might hinder fibrinolysis by suppressing AT III activity and Kallikrein activation, thus fostering thrombosis.[19–21] Nonetheless, the relevance of detecting aCL in stroke patients is underscored by the retrospective nature of our study, which primarily conducted aCL testing postthrombosis, suggesting aCL may develop subsequent to vascular injury from the stroke.[22,23]. The gene discussed is KLK4; the disease is Stroke.