Defects in CPT-1 and CPT-2 are associated with hypertriglyceridemia in humans [21], whereas increased CPT-1 activity is associated with reduced TG concentrations and reduced muscle- and liver steatosis in rats [22], suggesting that the high TG levels in the present study population is not caused by decreased β-oxidation. The gene discussed is CPT1A; the disease is hypertriglyceridemia.