Loss of the transcriptional activation function of LAP due to an increased LIP/LAP ratio was identified as a mechanism of evasion of the cytostatic response to TGF-β in metastatic breast cancer cells isolated from pleural effusions.18, 23, 24 The mechanism was traced to a role of C/EBPβ as a transcriptional activator of INK4b, a gene encoding the cyclin-dependent kinase inhibitor p15INK4b, which is an important mediator of growth inhibition in response to TGF-β.18 These data show that loss of C/EBPβ-mediated gene activation promotes breast cancer progression. This evidence concerns the gene CDKN2B and breast cancer.