PTPN22 is markedly overexpressed in CLL cells and may play a similar role in CLL pathogenesis as has been proposed for autoimmune diseases.57 In support of this possibility, experiments with primary CLL cells in vitro show that silencing of PTPN22 by RNA interference results in greater cell death following exposure to proapoptotic BCR stimuli, such as soluble anti-IgM.57 The capacity of PTPN22 to protect CLL cells from proapoptotic BCR stimuli is derived from its dual role in BCR signal transduction. The gene discussed is BCR; the disease is autoimmune disease.