When challenged with dietary (high-fat and high-carbohydrate diet) or genetic (leptin deficient and agouti induced) models of obesity, mice deficient for SCD1 displayed protection from fat accumulation and hepatic steatosis, thus highlighting the requirement of SCD1 to fully develop the obese phenotype peculiar of these models [82,96,122,125,126]. This evidence concerns the gene LEP and obesity disorder.