Thus, ALL survival could be indirectly promoted by bone marrow microenvironment-secreted Galectin-1, which could interact with glycoproteins on the surface of BP-ALL cells and promote chemotaxis: we found that inhibition of Galectin-1 by PTX008 reduced migration towards SDF1α and towards OP9 stroma. The gene discussed is LGALS1; the disease is acute lymphoblastic leukemia.