In mouse models, PDAC is driven by combined oncogenic KRAS mutation and haploinsufficient PTEN deficiency, which together promote marked NF-kB activation, its cytokine network (CCL20, CXCL1, IL-6, and IL-23), stromal activation, and immune cell infiltration; these processes shape the pancreatic cancer tumor microenvironment, stimulate the development of peritumoral stroma, and promote local and metastatic progression (Ying et al., 2011). This evidence concerns the gene KRAS and neoplasm.