Objective To analyze the relationship between polymorphism at the Apolipoprotein AI (Apo AI) gene and the risk for coronary artery disease. Methods A total of 107 patients (mean age 56 ± 11 years) diagnosed as having stable angina pectoris (SAP) (23 cases), unstable angina pectoris (UAP)(23 cases) or myocardial infarction (MI) (61 cases)were prospectively evaluated. DNA was obtained from the 107 patients and 50 controls. In order to determine the Apo AI genotypes at two polymorphic sites (G/A at -75 bp, and C/T at +83 bp), DNA was PCR amplified and digested with MspI. Results The frequency of carriers of the rare allele at the - 75 bp site (M1-) was 0.49 in cases and 0.30 in controls ( P＜ 0.05). The frequencies of the M 1 - allele among patients with SAP, UAP, MI and controls were 0. 37 (vs. Controls, P ＞ 0.05), 0. 54 (vs. Controls, P ＜0.05), 0.52 (vs. Controls, P＜ 0.05) and 0.30, respectively. The frequencies for carriers of the rare allele at the + 83bp polymorphism (M2) were observed among patients with SAP (0.09, vs. Controls, P ＞0.05), UAP (0. 11, vs. Controls, P ＞ 0.05) or MI (0.12, vs. Controls, P ＞ 0.05) and controls (0. 12).There was an slightly increase in the frequency of the M1 - allele in patients with SAP to UAP or MI (0.37vs. 0.54 vs. 0.52; all P ＞ 0.05) and M1 polymorphism as a risk factor for CAD (OR=3.74, P ＜0.05). In the + 83bp polymorphism there was no difference in the allelelic frequencies in cases and controls (0. 11 vs. 0. 12; P ＞ 0.05). There was no significant difference in the frequency of the M2- allele in patients with SAP to UAP or MI (0.09 vs. 0.11 vs.0. 12; all P ＞ 0. 05) and M2 polymorphism not as a factor for CAD ( OR = 0. 80, P ＞ 0. 05) Plasma lipoprotein values in patients with the allele M1 - and M2 - had no different levels than those homozygous for the M1+ andM2+ (P＞ 0.05). Conclusion M1polymorphism (M1 - ) may be as a risk factor for CAD and M2 polymorphism (M2 - ) not as a factor for CAD in Chinese Xinjiang Uygur and Han population.