Lee et al. discovered that AhR overexpression attenuated lung cancer invasion by inducing Smad4 ubiquitination and proteasome degradation after binding to Smad4 under non-ligand conditions in lung cancer cells, providing new insight into the role of AhR in cancer formation and a novel target for therapeutic intervention [93] (Fig. 2). The gene discussed is SMAD4; the disease is lung carcinoma.