We have therefore confirmed previously published literature showing that restoration of PAX5 levels rescues deficiency of PAX5 activity in pre-B ALL cells [18] and have shown for the first time that its paralogs, PAX2 and PAX8, demonstrate a high level of functional redundancy in downstream activation of B cell specific gene expression, promoting differentiation similar to that seen with PAX5. This evidence concerns the gene PAX2 and acute lymphoblastic leukemia.