AKT1 and pancreatic ductal adenocarcinoma: Studies in KRASG12D, sst2± hybrid mice demonstrated that PI3K/AKT signaling activates NF-κB signaling and activates KRAS, promoting the release of CXC chemokine ligand 16 (CXCL16) and IL-6, ultimately leading to the progression of pancreatic ductal adenocarcinoma (PDAC).112 The PI3K/AKT/NF-ΚB signaling system also facilitates the epithelial-mesenchymal transition (EMT).113