Telomere dysfunction in type II AECs, mediated by deletion of the telomere shelterin protein TRF1, leads to spontaneous development of pulmonary fibrosis in mice (SPC-creTRF1flox/flox mice). We sought to identify gene signature in these lungs in an effort to understand molecular mechanisms of the disease. Overall design: Tamoxifen was administered to SPC-creTRF1flox/flox mice and TRF1flox/flox littermate controls beginning at 8 weeks age. Lungs from SPC-creTRF1flox/flox mice were collected after 3 months and 9 months of tamoxifen administration whereas lungs from TRF1flox/flox controls were collected after 9 months of tamoxifen administration. This design is intended to identify gene changes at both early and late stage of the disease and compare with controls. Mouse whole lungs were harvested for RNA extraction and hybridization on one color Agilent microarrays.