Autoimmune cytopenias are a consequence of autoantibodies that target blood cell lineages and mark them for their accelerated destruction, mostly through phagocytosis by monocytes and macrophages and complement activation. Neutrophils, although equipped with Fc and complement receptors and effector mechanisms that are critical in other autoimmune conditions, remained long time overlooked. Recent reports however propose a new and possibly critical role for neutrophils. In this review we gathered available evidences on the contribution of neutrophils to the development, onset and consequences of autoantibody-dependent cytopenias.