This model indicates that type I and II IFNs promote the resistance to apoptosis of primary CLL cells through the simultaneous activation of TYK2 and Src, or JAK2 and Src kinases respectively, which in turn activate a STAT3/Mcl-1 signaling pathway, leading to the further modulation of both ΔΨm disruption, caspase-3 activation and DNA fragmentation. This evidence concerns the gene MCL1 and B-cell chronic lymphocytic leukemia.