Therefore it is conceivable that different B cells already present different telomere length before the leukemic transformation; alternatively, kinetic characteristics of CLL cells can determine differences in telomere length, and telomere shortening might be a consequence of 11q- or 17p- aberration that, together with ZAP-70, CD38 and CD49d overexpression, results in a more rapid CLL cell turnover, facilitating survival and cell-cycle progression [58,61]. The gene discussed is ITGA4; the disease is B-cell chronic lymphocytic leukemia.