The fact that restoration of DIO1 expression in ccRCC cells leads to attenuation of proliferation and migration [21] indicates that anti-oxidative response observed in this study could be inefficient and that oxidative stress generated by DIO1-induced acceleration of pro-tumorous metabolism could exceed antioxidative capacities of ccRCC cells, initiating mechanisms leading to cell death. Here, DIO1 is linked to nonpapillary renal cell carcinoma.