It is interesting that having a copy number of 0 has been reported much more frequently for FCGR3B than for FCGR3A, although the deletions of both genes are mediated by the same mechanism and having only 1 copy of either gene has been associated with immunological diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and anti-glomerular basement membrane antibody disease [9, 10, 12, 68–71]. This evidence concerns the gene FCGR3A and systemic lupus erythematosus.