Mice with Nrf2 deletions are inherently more susceptible to drug-induced toxicity and oxidative stress-induced diseases, including neurological diseases, while the overexpression of Nrf2 ameliorates the destructive effects of oxidative stress in various in vivo and in vitro disease models, including models of Parkinson's disease and HD (Copple, 2012; Joshi and Johnson, 2012; Suzuki et al., 2013). Here, NFE2L2 is linked to Huntington disease.