We therefore suggest that this adhesion inhibition is responsible for B-ALL cell susceptibility, based mainly on two facts: 1) We have shown that the soluble factors produced by MSC or by the co-cultures were unable to protect B-ALL cells from death; and 2) some of the adhesion molecules (VLA-5 and ICAM-1) expressed in MSC that have been implicated normally in interactions between MSC and both HSC and leukemic cells [46,47,48], and which we have shown to be upregulated during co-cultures with B-ALL cells, were importantly down-regulated by HKPS. The gene discussed is ICAM1; the disease is precursor B-cell acute lymphoblastic leukemia.