The survival of the neoplastic clone is supported by intrinsic defects of CLL cells, such as the activation of the B-cell receptor (BCR), the overexpression and activation of the Src kinase Lyn [8,9], Bruton tyrosine kinase (BTK) [10] and Bcl-2 [11] proteins, and extrinsic microenvironmental factors derived from the bone marrow or lymph nodes [12]. Here, BCL2 is linked to B-cell chronic lymphocytic leukemia.