Therefore, we hypothesized that epigenetic modification of the promoters of leptin, its receptor and satiety regulators in the hypothalamus may be the mechanism that causes leptin resistance, and an imbalanced intake of n-6/n-3 PUFAs (a higher intake of n-6 PUFAs and a lower intake of n-3 PUFAs) may influence the epigenetic modification of these promoters in obesity. This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.