This phenotype may be dependent on signaling through toll-like receptor (TLR) adaptor protein myeloid differentiation primary response gene 88 (MyD88), as B-cell-specific deletion of MyD88 from Lyn−/− B cells ameliorated auto-antibody production, T cell activation, myeloid expansion, and the development of glomerulonephritis (114). Here, LYN is linked to glomerulonephritis.