The mechanisms of chemoresistance of PDAC may involve the hypoxic tumor microenvironment and deficient vascularization, remodeled metabolism, the capacity for epithelial-mesenchymal transition and altered key signaling pathways, such as the PI3 K/Akt and NF-κB signaling pathways [19, 44–49]. This evidence concerns the gene AKT1 and neoplasm.