CD79A and myeloid sarcoma: Nevertheless, FCRL3 stimulation via secretory IgA has recently been shown to promote a pro-inflammatory phenotype, in part by inhibiting the suppressive effects of regulatory T cells45, as previously shown46, and the risk allele of the rs6681271 variant has been shown to increase FCRL3 expression39,47, consistent with an increased MS risk (assuming the increased expression promotes increased total FCRL3 stimulation on regulatory T cells).