Our data demonstrate that blockade of ATR activity in IFN-α–treated B cells was followed by a B cell profile that does not predispose to SLE, such as the reduction in antibody formation; of plasmablasts; and of soluble IL-10, IL-6, IL-4, and TNF-β and the increase of soluble IL-2, yet the released levels of BAFF were increased, while membrane-bound BAFF decreased. Here, ATR is linked to systemic lupus erythematosus.