To better understand the molecular mechanism by which the two inhibitors affect neoplastic B cell survival, we evaluated the phosphorylation status of Lyn (the tyrosine kinase that sustains the neoplastic clone survival through its constitutive activation) [30, 31] and ERK (a protein involved in BCR signaling, CXCL12/CXCR4 axis and responsible for the reduced apoptosis and the migration of CLL cells beneath stromal cells) [32]. This evidence concerns the gene CXCL12 and B-cell chronic lymphocytic leukemia.