In pancreatic cancers, mutational activation of KRAS or alterations in PI3K regulation caused by phosphatase and tensin homolog (PTEN) loss can enhance NF-κB activation and NF-κB-associated activation of downstream cytokine genes (including c-Myc and Cyclin D1) [39–43], and thus, contribute to progression of these tumors. This evidence concerns the gene KRAS and pancreatic neoplasm.