Along the same line, Pereira et al. [3] reported that B1R agonist exacerbated experimental focal and segmental glomerulonephritis (FSGS) but that B1R antagonist reduced proteinuria and glomerulofibrosis, reversed podocyte dysfunction, and played a protective role in the pathogenesis of FSGS. The gene discussed is BDKRB1; the disease is focal segmental glomerulosclerosis.