Among the leukocytes involved in the pathophysiology of SCA, neutrophils are particularly relevant, as these are the most abundant leukocytes in the circulation and, when activated, are recruited to vascular walls, in turn, forming aggregates with erythrocytes and/or platelets through interactions involving the integrin αMβ2 (Mac-1; CD11b/CD18)6,7. The gene discussed is ITGB2; the disease is autosomal dominant cerebellar ataxia.