Whether genomic instability facilitates the inactivation of p16Ink4A/p19Arf in ATM-deficient pancreatic tumor cells or other mechanisms are involved in p16Ink4A/p19Arf downregulation warrants further investigation (e.g., ATM loss could enable the DNMT1-mediated methylation of the p16Ink4A promoter)40. This evidence concerns the gene DNMT1 and pancreatic neoplasm.