Consistent with our hypothesis that EZH2 represses the p19Arf-p53wt axis, we observed increased p19Arf and p53 expression in KEC vs. KC PDAC precursor lesions (Figure 6A–C), suggesting that in the context of Ezh2 deficiency oncogene-induced failsafe programs are at least partially maintained in the Kras mutant pancreas. Here, EZH2 is linked to keratoconus.