Supporting this hypothesis are previous publications describing association of CNVs in FCGR3B and complement component 4 (C4A/C4B) with systemic lupus erythematosus (SLE), FCGR2C with idiopathic thrombocytopenic purpura (ITP), defensin beta (DEFB) with psoriasis and Crohn disease, CCL3L1 with HIV-AIDS infection, SLE, rheumatoid arthritis (RA) and type 1 diabetes (reviewed in [47]). This evidence concerns the gene FCGR2C and rheumatoid arthritis.