It arises as a desmoplastic tissue response which stems from crosstalk between tumor cells and the surrounding stroma, and is further driven by genetic mutations, notably in the KRAS oncogene but also including other factors such as the tumor suppressor genes TP53 and SMAD4, as well as the cell cycle regulator CDKN2A [8–10]. This evidence concerns the gene SMAD4 and neoplasm.