In lung cancer, most often showing TNKS overexpression, tumors possess abnormal Wnt activity, due to APC and β-catenin mutations, as well as to the deregulation of upstream Wnt signaling effectors, such as Dishevelled 3 (Dvl-3), or the downregulation of Wnt antagonists, as Wnt-inhibitory factor 1 (WIF 1). This evidence concerns the gene TNKS and lung carcinoma.