Background: In general, the metabolism of carcinogens involves two pathways. The oxidative pathway, which enhances carcinogenesis (phase I), and the protective pathway, in which carcinogens are conjugated with a series of substances such as glutathione to achieve detoxification (phase II). It has been suggested that an increased phase I enzyme activity (CYP1A1) and a decreased phase II enzyme activity (GST M1) could each individually cause an increase in the risk of cancer. Materials and Methods: In the present study we explored the association between genetic polymorphisms of CYP1A1 and GST M1 and non-small cell lung cancer (n = 55) and controls (n = 60) in Turkish subjects. We used PCR methods and enzyme restriction for determining polymorphism. A standard food questionnaire was used to determine daily fresh fruit consumption. Results and Conclusion: We found that CYP1A1 mutant variant (Ile/Val) was more highly expressed in Turkish patients and controls than in other Caucasian populations. Our findings were similar to Far Eastern populations (32.7% for patient group, 43.1% for controls). In spite of the similarity between the groups regarding GST M1 polymorphism, in the patient group, patients with GST M1 null genotype had a statistically significant positive history of exposure to carcinogens other than smoking, such as asbestos, petrochemicals and/or other chemicals (p = 0.01). The patients, who had CYP1A1 mutant variant, had increased risk of,adenocarcinoma (p = 0.046) of lung (8 out of 18 patients) and 6 of them also had GST M1 (-) gene variants together. The patients who consumed less fruit daily had a greater risk of epidermoid carcinoma of lung (p = 0.019). However this study showed that there were no differences between the patient and control groups regarding genetic polymorphism of genes.