"Pulmonary fibrosis (PF) is a progressively debilitating disease of unknown origin, with usual first presentation in 50’s plus age group. Over 500M people are afflicted by this disease world wide; however, this is an underestimate as incidence is rapidly rising as PF becomes better diagnosed. There is currently no efficacious therapeutic intervention which can either halt or reverse the disease process. Pulmonary Fibrosis carries a very poor prognosis of less than 3 years from diagnosis. Hence, PF morbidity and mortality imposes a huge socioeconomic burden as a chronic irreversible lung condition across the European Region, contributing significantly to the annual 102 billion Euros respiratory health cost and rising; most is due to hospital and community care support as well as early retirement / loss working days in those affected before 65yrs. There is a desperate unmet clinical need for PF patients across Europe and globally. PF thus presents a major therapeutic challenge. Recent research in PF pathogenesis suggests that inadequate regeneration of alveolar epithelium following presumed recurrent micro injury is a key factor in propagating development of fibrosis (over-scarring) within the lung. Whilst a number of plausible mechanisms may be responsible for this repair dysfunction in the alveolar epithelium, a likely hypothesis is that presence of a PF- related aberrant epithelial-mesenchymal transdifferentiation prevents a healthy epithelial cell – fibroblast balance. It follows that modulation of alveolar repair processes, and influence on fibro / myofibroblast transdifferentiation, represents a novel target in anti-PF therapeutics. Stem cells are at the centre of biomedical research for the treatment of many chronic debilitating diseases. We speculate that strategies involving use of human progenitor cells, such as autologous mesenchymal stem cells (hMSC), human embryonic stem cells (hESC) or their products for future treatment of lung fibrosis could be a"