Mice with a deletion of p62/Sqstm1 (p62-KO), a regulator of selective autophagy, show hyperphagia-induced obesity owing to abnormal leptin signaling, and develop a phenotype similar to that of metabolic syndrome in humans (Okada et al., 2009; Harada et al., 2013), including glucose intolerance, insulin resistance, and non-alcoholic fatty liver (NAFL). This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.