STAT3 and pancreatic ductal adenocarcinoma: This, in turn, led to activation of the Nuclear Factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Phosphorylated Signal Transducer and Activator of Transcription 3 (p-STAT3) pathways—both of which promote the development of preneoplastic lesions and carcinogenesis—along with the recruitment of additional inflammatory cells, ultimately accelerating the progression of pancreatic ductal adenocarcinoma [25].