Interestingly, IGF-1R could promote EMT, although committed mesenchymal-like lung, colon and pancreatic adenocarcinoma cells are no longer dependent on IGF-1R signalling for proliferation or survival (Barr et al, 2008), suggesting that, like EGFR, IGF-1R signalling is an important driver in epithelial cells and can induce EMT, but once these cells have transitioned to a mesenchymal state they are no longer reliant on IGF-1R, whereas alternate growth factor pathways could be activated following EMT. Here, EGFR is linked to pancreatic adenocarcinoma.