Our experimental data, together with recent results obtained on different cell lines (Orso et al, 2008), suggested that this anti-tumour activity resulted from a cell cycle arrest as we previously showed that the cyclin-dependent kinase inhibitor p27kip1 protein levels in pancreatic cancer cells were strongly increased after an AP-2α overexpression (Fauquette et al, 2007). Here, CDKN1B is linked to neoplasm.