Indeed, PAD patients with splenomegaly exhibited lower CD10 expression on PMN suggesting a more immature phenotype; on the other hand, patients with autoimmune manifestations exhibited a more activated phenotype (displaying an increased integrin CD11b and CD16 expression on isolated PMN), suggesting an enhanced potential for arrest on the endothelium (and subsequent extravasation), as well as an enhanced potential for phagocytosis. The gene discussed is FCGR3A; the disease is Splenomegaly.