For example, prolonged, non-canonical activation of the transcription factor NRF2 (nuclear factor erythroid 2-related factor 2), which results from autophagy inhibition, and p62-dependent sequestration of Keap1, the negative regulator of NRF2, has been shown to mediate insulin resistance and glucose intolerance in wild-type mice exposed to 25 ppm iAs for 20 weeks [167]. The gene discussed is NFE2L2; the disease is Glucose intolerance.