This model indicates that NGAL (by binding to NGAL-R) promotes the resistance to apoptosis of primary CLL cells through the sequential activation of an Src kinase, STAT3 and Mcl-1, leading to the further inhibition of both ΔΨm disruption, caspase-3 activation and DNA fragmentation. The gene discussed is STAT3; the disease is B-cell chronic lymphocytic leukemia.