In addition, Mac-1 attenuates FcγRIIA-dependent neutrophil recruitment in response to deposited immune complexes which is key to organ damage in a model of systemic lupus erythematosus and thus prevents excessive inflammation, demonstrating that Mac-1 has diverse and partially opposing roles in mammals (73, 74). The gene discussed is ITGB2; the disease is systemic lupus erythematosus.