Since inflammation predisposes to the development of cancer and promotes all stages of tumourigenesis [39] and DPT was previously described as a tumour suppressor molecule, our findings suggest a compensatory mechanism whereby DPT expression may increase in the context of strong inflammation, trying to avoid or minimize cell damage exhibiting its tissue-repairing functions; however, whether DPT is an inflammation driver or a responder still remains unknown. Here, DPT is linked to neoplasm.