In pancreatic ductal adenocarcinoma (PDAC), CAFs contribute particularly to chemotherapeutic resistance through various mechanisms such as secretion of growth factors and cytokines, inhibition of immune cell infiltration, activation of STAT3 signaling, upregulation of CXCR2, exosome secretion, microRNA signaling, and metabolic reprogramming [83–90]. Here, STAT3 is linked to pancreatic ductal adenocarcinoma.