For example, in the experimental murine model study of KRAS oncogene and tumor-specific TP53 missense mutation, oncogenic KRAS-driven cAMP responsive element-binding protein 1 (CREB1) phosphorylation by the MAPK/MEK pathway increased forkhead box protein A1 (FOXA1) upregulation and β-catenin stabilization, leading to the development of metastatic PDAC phenotypes [106]. Here, KRAS is linked to neoplasm.