Since we previously showed that increasing levels of endogenous Galectin-3 protein by overexpression from a retroviral vector protects pre-B ALL cells against drug treatment [6], we propose a model in which the induction of endogenous Galectin-3 protein production requires cell-to-cell contacts between stromal and ALL cells and is aided by chemotherapy (Suppl. The gene discussed is LGALS3; the disease is acute lymphoblastic leukemia.