In these patients, the neoplastic population expressed α4β1, which conferred the ability to adhere strongly to the stimulated endothelium via α4β1 ligand, vascular cell adhesion molecule 1 (VCAM-1) and concluded that constitutive integrin expression/function, intrinsic activation state of the cell and the ability of cytokines to modify integrin-mediated production are combined to determine the different clinical patterns of disease observed in lymphocytic leukemia [6,7,8]. The gene discussed is VCAM1; the disease is lymphoid leukemia.