The effect of B cell targeting therapies such as rituximab cannot be entirely explained by the reduction of autoantibody levels.26 FcRL4+ B cells express significantly higher levels of CD20 compared with other synovial B cells, and we have previously shown that following treatment of RA patients with rituximab, levels of RANKL in the synovium are significantly diminished.9 Removal of the FcRL4+ subset of B cells from the inflamed synovium may, therefore, contribute to the anti-inflammatory and ant-ierosive effect of rituximab. The gene discussed is TNFSF11; the disease is rheumatoid arthritis.