Similarly, human B-cell progenitors from Ph+ or Ph-like B-ALL patients, containing secondary pathogenic mutations (including loss of CDKN2A/B, mutant PAX5 and loss of IKZF1; see Supplemental Methods), show increased VAV3 expression with a predominant nuclear distribution (Fig. 1D, E). Here, VAV3 is linked to precursor B-cell acute lymphoblastic leukemia.