In addition, the role of SYK in the production of abnormal IgA1, and the autoantibodies directed against it, by B cells and plasma cells, has not been explicitly studied in IgA nephropathy, although data from other experimental immune models have suggested this may be a potential benefit, and other B-cell–directed therapies are undergoing clinical evaluation in IgA nephropathy. This evidence concerns the gene IGHA1 and IgA glomerulonephritis.