Next, we performed Cxcr4 blockade experiments (Figure 6A) in the mouse IgA glomerulonephritis model (16, 19), a transgenic mouse that expresses excessive BAFF, which exhibits features of autoimmune disease, including B cell hyperplasia and hypergammaglobulinemia, and develops IgAN with circulating immune complexes and immunoglobulin deposition in the kidney (Supplemental Figure 9). The gene discussed is CXCR4; the disease is IgA glomerulonephritis.