While most detected mutations are likely tobacco-associated TP53 mutations, others may suggest alternative oncogenesis mechanisms: notably we found MET, FGFR3, SMAD4 and CTNNB1 mutations, all genes that could potentially be involved in the lung fibrosis process, either participating to epithelial-mesenchymal transition or the regulation or TGFβ pathway. This evidence concerns the gene MET and pulmonary fibrosis.