Fil: González Guerrico, Anatilde M. Instituto de Investigaciones Bioquı́micas Fundación Campomar (UBA, CONICET), 1405 Buenos Aires; Argentina.Fil: Cafferata, Eduardo. ANLIS Dr.C.G.Malbrán. Centro Nacional de Genética Médica; Argentina.Fil: Radrizzani, Martín. ANLIS Dr.C.G.Malbrán. Centro Nacional de Genética Médica; Argentina.Fil: Marcucci, Florencia. Instituto de Investigaciones Bioquı́micas Fundación Campomar (UBA, CONICET), 1405 Buenos Aires; Argentina.Fil: Gruenert, Dieter. Human Molecular Genetics Unit, Department of Medicine, University of Vermont, Burlington; Estados Unidos.Fil: Pivetta, Omar H. ANLIS Dr.C.G.Malbrán. Centro Nacional de Genética Médica; Argentina.Fil: Favaloro, Roberto R. Fundación Favaloro, 1093 Buenos Aires; Argentina.Fil: Laguens, Rubén. Fundación Favaloro, 1093 Buenos Aires; Argentina.Fil: Perrone, Sergio V. Fundación Favaloro, 1093 Buenos Aires; Argentina.Fil: Gallo, Guillermo C. Hospital de Pediatrı́a Prof. Dr. Juan P. Garrahan, 1425 Buenos Aires; Argentina.Fil: Santa-Coloma, Tomás A. Instituto de Investigaciones Bioquı́micas Fundación Campomar (UBA, CONICET), 1405 Buenos Aires; Argentina.Cystic fibrosis (CF), a disease caused by mutations in the cystic fibrosis transmembrane regulator (CFTR) chloride channel, is associated in the respiratory system with the accumulation of mucus and impaired lung function. The role of the CFTR channel in the regulation of the intracellular pathways that determine the overexpression of mucin genes is unknown. Using differential display, we have observed the differential expression of several mRNAs that may correspond to putative CFTR-dependent genes. One of these mRNAs was further characterized, and it corresponds to the tyrosine kinase c-Src. Additional results suggest that c-Src is a central element in the pathway connecting the CFTR channel with MUC1 overexpression and that the overexpression of mucins is a primary response to CFTR malfunction in cystic fibrosis, which occurs even in the absence of bacterial infection.