Consistent with in vitro findings, despite the reduction in T-ALL burden, anti-VCAM-1 blocking antibodies did not reduce IGF1R or AKT activation in T-ALL cells from Icam1-/- mice (Supplementary Fig. 7b, c), suggesting ICAM-1 and VCAM-1-mediated integrin activation promote T-ALL survival through additional mechanisms beyond IGF1R activation in vivo. This evidence concerns the gene ICAM1 and acute lymphoblastic leukemia.