As TGF-β/Smad signalling has been shown to be a pro-tumorigenic factor in cutaneous melanoma and lung cancer25, 26, the role of Smad3 in tumour microenvironment was investigated by using two syngeneic mouse tumour models with luciferase-expressing invasive mouse lung carcinoma (LLC-luc) or melanoma (B16F10-luc) established in Smad3−/− (deletion of exon 8 and disruption of exon 710) and their littermate Smad3+/+ mice (C57BL/6J background). This evidence concerns the gene SMAD3 and lung carcinoma.