The mechanisms behind mitotane-induced dyslipidemia are multifactorial and include increased hepatic cholesterol synthesis via stimulation of HMG-CoA reductase; induction of hepatic cytochrome P450 enzymes, particularly CYP3A4, affecting HDL metabolism; impaired lipid clearance due to SR-B1 receptor modulation; inhibition of CYP11A1, reducing cholesterol conversion to pregnenolone; indirect effects of mitotane-induced hypothyroidism, which itself promotes hypercholesterolemia. The gene discussed is CYP3A4; the disease is metabolic syndrome.