Abstract: Objective To study the relationship between the antituberculosis drug-induced liver injury （ATDILI）and genetic polymorphism of drug metabolizing emzymes (DME)，including NAT2, GSTM1, GSTT1，and to illuminate the molecular mechanism of ATDILI.  Methods Of 208 inpatients in the initial treament of tuberculosis were admitted to the department of tuberculosis research, 309th Clinical Division of Chinese PLA, Amomg these patients 101 cases were with ATDILI while the other 107 cases without ATDILI were used as control. Polymorphisms of NAT2 were determined by polymerase chain reaction-direct sequencing(PCR-DS). The deletion in GSTM1 and GSTT1 genes was determined by multiplex PCR. Genotype frequencies were compared between cases and controls byχ² test using SPSS 12.0 software,Odds ratio (OR) and 95% confidence interval(95%CI) were calculated to analyze the relationship between genotypes and ATDILI.  Results （1）There were 40 patients with slow acetylator (39.6％) in 101 cases with hepatotoxicity and 13 with slow acetylator (12.2％）in 107 controls without hepatotoxicity. Patients with slow acetylator genotype (OR＝4.74, 95%CI:2.42-9.28; χ²=20.62, P<0.05) had a significantly higher risk of antituberculosis drug-induced hepatotoxicity than those with rapid or intermediate acetylator genotypes. (2) There were 64 patients with GSTM1 null genotype(63.4％) in cases with hepatotoxicity and 55 with GSTM1 null genotype (51.4％）in controls without hepatotoxicity. The GSTM1 null genotype (OR=1.64, 95％CI=0.94-2.84,χ²=3.038，P>0.05) had higher risk of ATDILI than GSTM1 non-null genotype no statistical significance).There were 48 patients with slow acetylator (47.5％) in cases with hepatotoxicity and 49 with slow acetylator (45.8％）in controls without hepatotoxicity, (OR=1.07, 95％CI=0.62-1.85,χ²=0.063，P>0.05). (3) The patients with slow acetylator genotype of NAT2 combined with GSTM1 null genotype(OR=10.21, 95%CI=3.87-26.96，χ²=20.62，P<0.005) had higher risk of ATDILI than those only with slow acetylator genotype (OR=4.74, P=0.000) or with GSTM1 null genotype (OR=1.64, P>0.05).  Conclusion The slow acetylators of NAT2 and the GSTM1 null genotype might be associated with ATDILI.