Supplementation with N-acetylcysteine (NAC), the precursor of GSH, early after DEN administration has proven to mitigate DEN-induced HCC tumor growth in mice through maintaining adequate levels of GSH and GST, without affecting the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), a key up-stream transcription factor of GSH metabolism and antioxidant capacities [8]. Here, NFE2L2 is linked to neoplasm.