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Tuberculosis is a worldwide health problem, as an increasing threat with the spread of HIV infection and drug resistant Mycobacterium tuberculosis strains.Isoniazid (INH) and rifampin (RFP) are the backbone of the standard regimen for treating tuberculosis(TB), and resistance to these drugs indicates a necessity for alteration of the standard regimen.Increasing prevalence of INH resistance, especially in high tuberculosis (TB) prevalent countries is worsening the burden of TB control programs.It is reported that rpoB gene was associated with rifampin resistance, and mutations in the 81bp rifampin resistance determining region(RRDR) induce resistance to rifampin(RFP).Whereas the molecular basis for isoniazid(INH) resistance in Mycobacteriwn tuberculosis is complex.Putative isoniazid resistance mutations have been identified in katG, ahpC, inhA, kasA, and ndh.However, resistance in Mycobacterium tuberculosis to isoniazid (INH) is most caused by mutations in the catalase-peroxi-dase gene (katG).