Collectively, these data raise the possibility that innate immunity boosting might represent a viable strategy for risk reduction or prevention in childhood-related B-ALL; early innate immune response induction by Myd88-independent Toll-like receptor ligation during the preleukemic phase in Pax5+/− mice resulted in significant delay of B-ALL development under oncogenic environmental conditions, supporting the view that immune modulation during the preleukemic stage can significantly alter progression to B-ALL. Here, MYD88 is linked to precursor B-cell acute lymphoblastic leukemia.