Thus, PC is not characterized by a lack of specific T-cell immunity but by a potent barrier established by complex cancer-stroma interactions that inhibit T-cell activity in situ; for this purpose is most explanatory the recent results obtained by De Monte et al. [39]; they showed that thymic stromal lymphopoietin (TSLP), which favors Th2 cell polarization through myeloid DC conditioning, was secreted by cancer-associated fibroblasts (CAFs) after activation with tumor-derived TNF-α and IL-1β. This evidence concerns the gene IL1B and cancer.