We therefore undertook additional genotyping in our original RA cohorts and examined SNPs in FCGR2A, FCGR2B and FCGR3B; examined the extent of linkage disequilibrium at this locus; and analyzed FCGR haplotypes for association with disease in order to investigate the possibility that there are other RA susceptibility variants at this locus. This evidence concerns the gene FCGR2B and rheumatoid arthritis.