The present study aimed to investigate the association of g.313A>G\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.313\hbox {A}{>}\hbox {G}$$\end{document} and g.341C>T\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.341\hbox {C}{>}\hbox {T}$$\end{document} polymorphisms of GSTP1 with coronary artery disease (CAD) in a subgroup of north Indian population. In the present case–control study, CAD patients (n=200\documentclass[12pt]{minimal}
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\begin{document}$$n = 200$$\end{document}) and age-matched, sex-matched and ethnicity-matched healthy controls (n=200\documentclass[12pt]{minimal}
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\begin{document}$$n = 200$$\end{document}) were genotyped for polymorphisms in GSTP1 using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Genotype distribution of g.313A>G\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.313\hbox {A}{>}\hbox {G}$$\end{document} and g.341C>T\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.341\hbox {C}{>}\hbox {T}$$\end{document} polymorphisms of GSTP1 gene was significantly different between cases and controls (P=0.005\documentclass[12pt]{minimal}
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\begin{document}$$P = 0.005$$\end{document} and 0.024, respectively). Binary logistic regression analysis showed significant association of A/G (odds ratio (OR): 1.6, 95% CI: 1.08–2.49, P=0.020\documentclass[12pt]{minimal}
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\begin{document}$$P = 0.020$$\end{document}) and G/G (OR: 3.1, 95% CI: 1.41–6.71, P=\documentclass[12pt]{minimal}
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\begin{document}$$=$$\end{document} 0.005) genotypes of GSTP1 g.313A>G\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.313\hbox {A}{\!>\!}\hbox {G}$$\end{document}, and C/T (OR: 5.8, 95% CI: 1.26–26.34, P=0.024\documentclass[12pt]{minimal}
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\begin{document}$$P = 0.024$$\end{document}) genotype of GSTP1 g.341C>T\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.341\hbox {C}{>}\hbox {T}$$\end{document} with CAD. The A/G and G/G genotypes of g.313A>G\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.313\hbox {A}{>}\hbox {G}$$\end{document} and C/T genotype of g.341C>T\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.341\hbox {C}{>}\hbox {T}$$\end{document} conferred 6.5-fold increased risk for CAD (OR: 6.5, 95% CI: 1.37–31.27, P=0.018\documentclass[12pt]{minimal}
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\begin{document}$$P = 0.018$$\end{document}). Moreover, the recessive model of GSTP1 g.313A>G\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.313\hbox {A}{>}\hbox {G}$$\end{document} is the best fit inheritance model to predict the susceptible gene effect (OR: 2.3, 95% CI: 1.11–4.92, P=0.020\documentclass[12pt]{minimal}
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\begin{document}$$P = 0.020$$\end{document}). In conclusion, statistically significant associations of GSTP1 g.313A>G\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.313\hbox {A}{>}\hbox {G}$$\end{document} (A/G, G/G) and g.341C>T\documentclass[12pt]{minimal}
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\begin{document}$$\hbox {g}.341\hbox {C}{>}\hbox {T}$$\end{document} (C/T) genotypes with CAD were observed.
