In this context, the current result that CD40 co-stimulation can render AID dysfunctional B cells susceptible to BCR stimulation and that CD40 treatment of SLE B cells diminished the expression of, e.g., PTPN22 further support that modulation of the CD40 pathway is of critical importance in regulating B cell function at many levels. This evidence concerns the gene PTPN22 and systemic lupus erythematosus.