Gd-IgA1 is recognized as self-antigen and forms nephritogenic immune complexes with anti–Gd-IgA1-IgG, IgA, and/or IgM.12 Subsequent deposition of these circulating IgA-containing immune complexes in the glomerular mesangium instigates several injury pathways, resulting in glomerular inflammation and fibrosis. The gene discussed is IGHA1; the disease is inflammatory response.