However, mutations were preferentially targeted to the same regions of the IgGHV segment in RA and control donors, and there were no inter-group differences in the targeting of mutation (10) prevalence of IgGhypoM in RA donors did not result from AID or mismatch repair enzyme impairment or to the mono- or oligo-clonal expansions of IgG+ve BCRs with few mutations Supplementary Figures 6, 7. This evidence concerns the gene AICDA and rheumatoid arthritis.