In this manner, the moderate loss of hepatic Ceacam1 expression (by <50%) by NEFA release before overt insulin resistance develops in adipocytes (such as the case in uncomplicated moderate obesity—[89]) provides a positive feedback mechanism on fatty acid β-oxidation to limit hepatic steatosis in the early phases of increased energy intake and before chronic hyperinsulinemia develops [95]. The gene discussed is CEACAM1; the disease is Hyperinsulinemia.