On the basis of our present results, RUNX2 knockdown enhanced GEM sensitivity of AsPC-1 cells accompanied by further accumulation of TAp63 as well as a subset of its target genes in response to GEM, implying that RUNX2-mediated trans-repression of TAp63 has a pivotal role in the regulation of GEM-resistant phenotype of p53-deficient pancreatic cancer cells (Figure 1). Here, TP53 is linked to pancreatic neoplasm.