TLR9 and glomerulonephritis: Finally, a deficiency of A20 leads to an hyperactivation of B cells after BCR, LPS or CD40 activation and to the spontaneous production of autoantibodies but, similar to Carabin deficiency, an A20 defect is associated with the development of glomerulonephritis after TLR9 stimulation (Chu et al, 2011; Tavares et al, 2010).