The activation of this transcription factor can thus redirect glucose and glutamine into anabolic pathways [33]; ii) the p62-Keap1–Nrf2 axis also promotes malignancy of HCC through similar, but not the same, metabolic reprogramming, as it enhances UDP-glucuronate and glutathione production, which have been shown to stimulate HCC growth [56,57]; moreover, the concomitant Nrf2 activation and p62-mTORC-mediated c-myc activation [48] could be another mechanism conferring a selective advantage to HCC cells in comparison to cells where NRF2 activation is due to activating mutations. This evidence concerns the gene NFE2L2 and hepatocellular carcinoma.