Inflammation and cellular stress, such as hypoxia and oxidative stress, are intrinsic to tumor microenvironments and are particularly prevalent in pancreatic ductal adenocarcinoma (PDAC).1,2 Importantly, both stress and inflammation have been reported to promote tumor initiation, progression, and drug resistance.3,4 The Janus kinase (JAK) and signal transducer and activator of transcription 3 (STAT3) pathway facilitates cellular responses to extracellular signals such as cytokines, chemokines, and various forms of cellular stress. This evidence concerns the gene STAT3 and pancreatic ductal adenocarcinoma.