This is because deterioration of Nrf1α−/−-tumor results from hyper-active Nrf2, along with decreased PTEN and activation of downstream PI3K-AKT signaling, but the Nrf1/2+/+-tumor growth is unaffected by constitutive activation of Nrf2 when compared with caNrf2ΔN-tumor. This evidence concerns the gene PTEN and neoplasm.