It has been proposed that unmutated surface immunoglobulins in CLL are more responsive to antigenic stimulation, resulting in strong BCR-mediated signal transduction and induction of anti-apoptotic proteins such as XIAP and MCL-1 [11]–[13], while CLL cells with mutated IGHV more closely resembles anergic B cells [14], with incomplete responsiveness through the BCR pathway and induction of tolerogenic signals. Here, BCR is linked to B-cell chronic lymphocytic leukemia.