In pancreatic ductal adenocarcinomas (PDACs), dysregulation of β-catenin and the transcriptional activator FOXM1 mediates oncogenesis, although the underlying mechanism remained unclear until Li et al.[75] showed that loss of Smad4 in PDAC cells leads to reduced levels of miR-494, increased levels of FOXM1, and nuclear localization of β-catenin. Here, FOXM1 is linked to pancreatic ductal adenocarcinoma.