Taken together, our present findings strongly suggest that RUNX2 attenuates TAp63-dependent cell death pathway in p53-deficient pancreatic cancer cells following GEM exposure, and thus the depletion of RUNX2 might be an attractive strategy to enhance the efficacy of the clinically approved GEM, which contributes to save cost to treat patients with advanced pancreatic cancer when compared with the development of novel anticancer drug(s) targeting pancreatic cancer.12 Here, RUNX2 is linked to pancreatic neoplasm.