Patients with thrombo-inflammation (including stroke, sepsis, and SCD) all present with abnormal circulating platelet–leukocyte aggregates (with platelets binding to neutrophils in a P-selectin-dependent mechanism, an interaction that primes the leukocyte and promotes integrin activation), increasing their propensity to develop disseminated intravascular coagulation [49]. This evidence concerns the gene SELP and Stroke.