BCL2 and glomerulonephritis: Mice that constitutively express the prosurvival protein, Bcl2, only in B cells that have expressed activation-induced cytidine deaminase have decreased expression of activated caspase 3, higher numbers of mature plasma and memory B cells, produce autoantibodies, and spontaneously develop glomerulonephritis with associated moribundity, suggesting that Bcl2-mediated release of GC apoptosis enhances spontaneous autoimmunity (35).