PPARG and coronary artery disorder: After dividing into population source, the CAD risk magnitude of H-B studies was distinctly strengthened under the recessive model (P = 0.03, OR = 1.85, 95%CI 1.07–3.19, Pheterogeneity = 0.87, I2 = 0%) and the homozygote comparison (P = 0.03,OR = 1.83, 95%CI 1.06–3.16, Pheterogeneity = 0.88, I2 = 0%) (Figure 4), whereas in P-B subjects, the lack of remarkable association was found between the PPARγ2 Pro12Ala polymorphism and CAD under all genetic models (allele comparison: P = 0.64, OR = 1.03, 95%CI 0.93–1.14, Pheterogeneity = 0.10, I2 = 38%).