Although BCL-2 overexpression greatly accelerates lymphomagenesis in Eμ-Myc transgenic mice,25 endogenous BCL-2 is dispensable for MYC-driven lymphoma development.28 In contrast, BCL-XL was found to be essential for the survival of both normal as well as c-MYC overexpressing B-cell progenitors and its loss therefore inhibited lymphoma development in Eμ-Myc mice.29 Here we show that MCL-1 is also critical for c-MYC-driven lymphoma development. Here, BCL2 is linked to lymphoma.