By providing a first mechanistic and important insight into epigentic regulation of CSR to IgA expression, our findings open new avenues of investigation of the role of miR-146a-mediated IgA dysregulation in a variety of hyper IgA conditions, such as those in HIDS, “idiopathic” hyper IgA, autoimmune and non-autoimmune inflammatory diseases, cancer and select metabolic disorders. The gene discussed is CD79A; the disease is hyperimmunoglobulinemia D with periodic fever.