While it was shown that the concurrent expression of AID and RAG1 in small pre-BII cells contributes to the clonal evolution of childhood ALL in the presence of strong inflammatory stimuli [8], absence of AID expression in pre-BI and immature B-cells has been reported to confer implications in the control of self-tolerance, as shown in both mice and humans [20–25]. The gene discussed is RAG1; the disease is acute lymphoblastic leukemia.