Taking into consideration the fact that BCR-ABL overexpression mimics BCR signaling and since enhancement of the signaling cascade downstream of BCR-ABL leads to cell death (12, 42, 43), the activation of BAFFR-dependent signals in pre-B ALL cells might add-up to the tyrosine kinase activity of BCR-ABL (e.g., interfering with other major signaling pathways such as that of PI3K) and provide a rationale for BAFF-induced cell death of these cells. Here, BCR is linked to acute lymphoblastic leukemia.