To investigate the effect of simultaneous loss of endogenous Galectin-3 and Galectin-1 function on BCP-ALL cells, we transformed primary B-lineage murine bone marrow Lgals1 × Lgals3 -/- (hereafter referred to as dKO) and wild-type (wt) cells [56] with the p190 Bcr/Abl oncogene to generate an aggressive, well-proliferating B-cell precursor ALL [57] that does not depend on stromal support. This evidence concerns the gene LGALS1 and acute lymphoblastic leukemia.