Nevertheless, our findings, taken together, demonstrate that Pax5-dependent B-ALLs are profoundly affected by the proleukemic inflammatory environment in which leukemic progenitor cells reside, and also support the view that increased levels of the pro-inflammatory cytokine IL-6 are an essential trigger of the B-ALL disease observed in Pax5+/- mice. This evidence concerns the gene PAX5 and precursor B-cell acute lymphoblastic leukemia.