PAX5 and precursor B-cell acute lymphoblastic leukemia: We have recently shown that natural exposure to infectious pathogens contribute to the ‘‘switch’’ from a preleukemic state to a leukemic state in cells bearing these PAX5 mutations9,13, and Pax5 mutant mice go on to develop B-ALL with modest penetration when they are exposed to natural infections9, usually associated with the inactivation of the other copy of Pax5. In this context, inflammation has been hypothesized to play an essential role14–16, but precisely how inflammatory signals influence the Pax5 mutant B-cell leukemogenesis process is poorly understood.