Given the role of increased sphingolipids in the pathophysiology associated with obesity and AA as precursor to key inflammatory mediators, n-6 eicosanoids, prostaglandins and leukotrienes [32], it is conceivable that some of the beneficial effects related to the pharmacological and genetic inhibition of SCD1 reported in the context of obesity [33–35] are due to the reduction of those metabolites. This evidence concerns the gene SCD and obesity disorder.