PDX1 and neoplasm: Nonetheless, the capacity of Pdx1-Cre; LSL-KrasG12D/KrasWT mice to initiate tumours and develop high-grade pancreatic lesions despite wild-type p53 and intact p19ARF expression (Fig. 9c) supports the existence of non-genetic mechanisms to evade p19ARF-p53-mediated tumour suppression.