As increased oxidative stress has been described in HFD-induced obesity and it has been proposed that it may be associated with the accompanying insulin resistance, a plausible hypothesis would be that deletion of Nrf2 leads to increased oxidative stress in tissues (e.g. liver, adipose tissue, muscle) and exacerbates the resulting metabolic phenotype. Here, NFE2L2 is linked to obesity due to melanocortin 4 receptor deficiency.