Zgheib et al. 2013 studied the association of xenobiotic metabolizing genes and breast cancer risk by calculating the frequency of CYP2E1*5B (rs3813867 and rs2031920), CYP2E1*6 (rs6413432), NAT2*5 (rs1799929), NAT2*6 (rs1799930), GSTP1 6624 A>G (rs1695), GSTM1 215bp deletion, and GSTT1 480bp deletion in 227 breast cancer patients of Lebanese origin. The control group included in the study consisted of 99 unrelated women without breast cancer. No significant statistical differences were observed in the variant distribution of xenobiotic metabolizing genes between cases and controls.

Salem et al. 2011 investigated the GSTM1 and GSTT1 genotype frequencies in Bahraini, Lebanese, and Tunisian Arabs using multiplex PCR-based methods. GSTM1 and GSTT1 wild or null genotypes were determined in 167 Bahraini, 141 Lebanese, and 186 Tunisian subjects by identifying the presence of specific DNA bands on 1.5% agarose gel. Comparable GSTM1 null genotype frequencies were observed among Bahraini (49.7%) and Lebanese (52.5%) subjects. Tunisians had a slightly higher frequency of GSTM1 null genotype (63.4%). GSTT1 null genotype frequency among Bahraini subjects (28.7% ) were observed to be lower compared to that of Lebanese (37.6%) and Tunisians (37.1%) subjects. Statistically significant difference in frequencies noted in this study while comparing Bahraini and Tunisian GSTM1 null genotypes was attributed to the ethnic diversity observed in those populations.

Bu et al. (2004) studied the frequencies of alleles and genotypes for CYP1A1, NAT2, GSTs, MTHFR, MTR (MS), and NQO*1 genes among Arabs.  Of the studied group, 95% were from Saudi Arabia, and 5% were from Jordan, Syria, Lebanon, and Yemen.  The mean age was 37 years, and male to female ratio was (25:1).  The frequencies of the null genotypes for the GSTT1 and GSTM1 genes were 25 and 55%, respectively.  The frequency of the 1578G allele was 40% and that of the 2293T allele was 13% among Arabs.

Abu-Amero et al. (2006) examined the association between GSTT1 and GSTM1 deletion and coronary artery disease among smokers.  Using multiplex polymerase chain reaction, a total of 1054 Saudi CAD patients and 762 Saudi controls were genotyped.  A significant association was found between the T null M null, T null M mild, and T mild M null genotypes with CAD independent of smoking interaction.  In CAD patients 30% had the T wild M wild genotype, 27% had the T wild M null genotype, 8% had the T null M wild genotype, and 36% had the T null M null genotype.  Also smoking, age, hypercholesterolemia and hypertriglyceridemia, diabetes mellitus, family history of CAD, hypertension, and obesity where all associated with CAD. Few years later, Abu-Amero et al. (2009) investigated the prevalence of GSTM1 and GSTT1 deletion genotypes in spontaneous optic neuropathies.  A total of 108 Saudi patients with optic neuropathies and 120 control individuals, also Saudis, were included in the study.  All three GST deletion phenotypes (T0M1, T1M0, and T0M0) were found to be significantly more prevalent among the patient group than the control.  In addition, at least one deletion genotype was significantly greater for each type of spontaneous optic neuropathy.  Abu-Amero et al. (2009) suggested that GST deletion phenotypes may be involved in the pathogenesis of these optic neuropathies by way of the role that GST plays in detoxifying endogenous compounds and in inactivating endogenous end products formed during oxidative stress.

Al-Achkar et al. (2014) we investigated the associations of polymorphisms in the cytochrome P450 gene (CYP1A1) and the glutathione S-transferase genes (GSTM1 and GSTT1) with chronic myelogenous leukemia (CML).  A total of 126 patients with CML and 172 healthy volunteers were genotyped.  Logistic regression analyses showed significant risk of CML associated with CYP1A1 Val allele [odds ratio (OR) 3.3, 95% confidence intervals (CI) 1.96-5.53], (p < 0.0001) while CYP1A1 Val/Val homozygotes were observed only in the CML patients.  There was statistically significant difference in the frequency of GSTM1 and GSTT1 null genotypes.  The GSTT1-null genotype was slightly higher in 27% of CML cases and 17% of controls (OR 1.98, 95% CI 1.12-3.5) (p < 0.020).  The GSTM1 null was higher in 43% of CML cases and 23% of controls (OR 2.55, 95% CI 1.54-4.22) (p < 0.00024).  Individuals carrying the CYP1A1 Ile/Val (AG) and GSTM1 null genotype have 9.9 times higher risk to be CML than those carrying CYP1A1 Ile/Ile (AA) and GSTM1 present genotype (OR 9.9, 95% CI 2.7-36.3) (p < 0.0001).  Al-Achkar et al. (2014) concluded that the association of the GSTM1 null genotype, either alone or in combination with GSTT1 null, with CYP1AI heterozygous leads to the CML risk.

Khedhaier et al. (2003) carried out a case-controlled study to investigate the susceptibility and prognostic implications of the GSTT1 gene deletion in breast carcinoma. The GSTM1 gene was also investigated in this study. The variation of the GSTT1 and GSTM1 genes were characterized in 309 unrelated Tunisian patients with breast carcinoma and 242 healthy control subjects. A significant association was found between gene deletion of GSTT1 and the risk of early onset of breast carcinoma (OR=1.60, P=0.02). The lack of GSTT1 gene deletion was found to be significantly associated with poor clinical response to chemotherapy (OR=2.29, P=0.03). This association was found to be significantly higher in patients with axillary's lymph node-negative breast carcinoma (OR=12.60, P=0.005). The null-GSTT1 genotype showed a significant association with increased DFS in this selected population of patients. This association was found even higher in patients carrying both null-GSTT1 and -GSTM1 genotypes. Khedhaier et al. (2003) concluded that the GSTT1 gene deletion may predict not only the early onset of breast carcinoma but also the clinical response to chemotherapy and the recurrence-free survival for patients with lymph node-negative breast carcinoma.

In order to test the hypothesis that genetic polymorphism of glutathione S-transferase theta 1 (GSTT1) and/or glutathione S-transferase mu 1 (GSTM1) is associated with COPD in smokers, Faramawy et al. (2009) carried out a case-control study on 34 patients with COPD and 34 matched controls. Results indicated a carrier frequency of null GSTT1 genotype in 50% among cases compared to 44.1% in the control group. Carriers of null GSTT1 were found to be at minor risk of developing COPD when compared with carriers of the wild GSTT1 genotype (OR, 1.3; 95% CI, 0.5-3.3). In case of GSTM1, the frequency of carriers of null GSTM1 genotype was found to be 52.9% among cases compared to 26.5% in controls. Carriers of null GSTM1 were found to be at much higher risk of developing COPD (OR, 3.13; 95% CI, 1.1-8.6). Furthermore, Faramawy et al. (2009) found that the risk of developing COPD was increased among carrier of null GSTT1 and GSTM1 haplotypes (OR, 3.6; 95% CI, 1.1-11.6). Faramawy et al. (2009) concluded that carriers of null GSTM1 genotype were at high risk of developing COPD especially when they were null GSTT1 and GSTM1 haplotype.

Hussain et al. (2012) compared the frequency of GSTT1 gene deletion between 30 hypertensive patients (30 patients) and non-hypertensive individuals (33 controls). This study found no significant association between the null GSTT1 genotype and hypertension, and, therefore, concluded that null GSTT1 was not a significant risk factor for hypertension.