Mitochondrial dysfunction is marked by a diminished capacity for fatty acid oxidation, which is evidenced by decreased carnitine palmitoyltransferase 1 (CPT1) activity, increased uncoupling, elevated ROS levels, and exacerbated inflammatory responses.[36] This pathological change is a key driver in the progression of NAFLD/nonalcoholic steatohepatitis (NASH) and insulin resistance, often preceding the emergence of clinical symptoms. The gene discussed is CPT1A; the disease is metabolic dysfunction-associated steatohepatitis.