UM-CLL cells generally retain the ability to transmit signals through their BCR in comparison with M-CLL cells [20], with sustained BCR cross-linking resulting in a phosphoinositide 3-kinase (PI3K)/Akt-mediated up-regulation of Mcl1, which has been shown to increase CLL cell chemoresistance [21–23]. This evidence concerns the gene MCL1 and B-cell chronic lymphocytic leukemia.