Dexamethasone-induced insulin resistance remains a complex mechanism [15] that is suggested to involve changes in whole body free fatty acid turnover, plasma insulin concentrations [16] and alterations in both insulin signal transduction [17] and glucose transporters [18] Both leptin and adiponectin promote catabolic energy generating processes, such as the mobilisation of triglycerides stores to promote fatty acid oxidation [19]. The gene discussed is INS; the disease is Insulin resistance.