The dramatic decline of eGFP expression in the adult lung of the BRE-eGFP reporter mice and the association of eGFP expression with the epithelial progenitor pool prompted us to investigate whether the reporter was reactivated in adult lung during injury and repair. Adult BRE-eGFP animals were analysed in two established models of lung tissue injury and repair, namely the naphthalene and bleomycin induce lung injury models. Naphthalene treatment causes selective depletion of Clara cells in the airways [59] . In contrast, bleomycin causes epithelial cell death, acute inflammation and fibro-proliferative remodeling of the peripheral lung [60] . Immuno-staining for CC10 and CGRP demonstrated that by day 3, naphthalene treatment had caused a large reduction in CC10 pos cells in the airways, an increase in the number of CGRP pos cells per NEB, and a substantial increase in BRE-eGFP reporter activity at airway branch-points and terminal bronchioles ( Figure 8A ).This pattern of CC10 localization and eGFP reporter expression corresponds with previously determined anatomic locations that maintain chemically resistant epithelial progenitor cells [61, 62, 63, 64] .