SOAT1 and pancreatic ductal adenocarcinoma: While the putative down-regulation of TGF-β signaling has been previously considered controversial, with respect to the classical “molecular phenotype” of myofibroblasts related to CAFs, more recently, Biffi et al. [36] have highlighted differences in CAFs subpopulation in pancreatic ductal adenocarcinoma, discerning between two subtypes characterized by either myofibroblastic or inflammatory phenotypes, with the latter expressing Lif and JAK/STAT activation [36].