As GEM-mediated accumulation of TAp63 in RUNX2 knockdown cells remarkably stimulated the expression of a subset of p53/TAp63-target gene products including cell cycle-related p21WAF1 and pro-apoptotic NOXA, it is highly likely that RUNX2 contributes at least in part to the acquisition and/or maintenance of GEM-resistant phenotype of p53-deficient pancreatic cancer cells through the downregulation of TAp63-dependent cell death pathway. Here, RUNX2 is linked to pancreatic neoplasm.