In contrast, the exposure of SPF-housed Pax5+/− mice to an Myd88-independent TLR ligand (mice treated with an intravenous injection of 200 μg of poly(I:C) for a total of 2 times, separated by four weeks between doses) did not generate B-ALL (Fig. 4), therefore supporting the direct participation of Myd88 modulation in B-ALL development in this model. This evidence concerns the gene PAX5 and acute lymphoblastic leukemia.