Objective. To investigate the effect of apolipoprotein B (apoB) and E (apoE) genetic variations on lipid profile at baseline (before treatment), and also on the subsequent response to simvastatin therapy.Methods. Eighty-eight patients with hyperlipidemia were treated with simvastatin 5mg daily. The plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and apo B were measured pre-treatment and at the end of the 4th, 8th and 12th post-treatment week. Polymorphisms of apoB at XbaI locus and apoE were determined by restriction fragment length polymorphism (RFLP).Results. In all patients, relative frequencies of X- allele and X + allele were 0. 943 and 0. 057 for apoB gene respectively. For apoE gene the relative frequency of ε 2 allele was determined as 0. 182, ε3 as 0. 580 and ε4 as 0. 238. The reduction in TC level was more prominent in patients carrying X- allele than in those with X + allele following treatment (-23. 9% vs. -13. 6% , P < 0. 05). Co Objectives. To investigate the effect of apolipoprotein B (apoB) and E (apoE) genetic variations on lipid profile at baseline (before treatment), and also on subsequent responses to simvastatin therapy. Methods. Eighty-eight patients with hyperlipidemia were treated with simvastatin 5 mg daily. The plasma levels of total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C), triglyceride (TG) and apo B were measured pre-treatment and at the end of the 4th, 8th and 12th post- treatment week. Polymorphisms of apoB at XbaI locus and apoE were determined by restriction fragment length polymorphism (RFLP). Results. All patients, relative frequencies of X-allele and X + allele were 0. 943 and 0. 05 for apoB gene . For apoE gene the relative frequency of ε 2 allele was determined as 0. 182, ε3 as 0. 580 and ε4 as 0. 238. The reduction in TC level was more prominent in patients carrying X- allele than in those with X + allele following treatment (-23. 9% vs. -13. 6 %, P <0.05). Co