Here, we demonstrate that a COX‐2 inhibitor, celecoxib, alleviates hepatic steatosis and the inflammatory response in a non‐nutrient‐induced mouse model of NAFLD featuring increased de novo lipogenesis via the hydrodynamic transfection of the activated form of AKT, also known as protein kinase B (PKB), a conserved threonine/serine kinase for genome stability, nutrient availability and cellular energy metabolism. The gene discussed is AKT1; the disease is fatty liver disease.