laboratory contamination or failed sputum culture and DNA extraction. Of the final 309 GeneXpert-positive included participants, 200 (65%) were male (Table 1), 118 were RS and 191 were RR, and all had phenotypic DST successfully completed. RR was strongly associated with a history of TB treatment (p<0.0001) .Genomic profiling of Mycobacterium tuberculosis strains, Myanmar, comparing discriminatory power offered by GeneXpert (Cepheid, https://www.cepheid.com) and additional genotypic testing, such as line-probe assay or whole-genome sequencing. RIF resistance and sensitivity were determined by using the Xpert MTB/RIF assay (Cepheid). INH, isoniazid; MDR, multidrug resistant; RIF, rifampin; RR, rifampin resistant; RS rifampin sensitive; XDR, extensively drug resistant. *Resistance profile confirmed by phenotypic testing.. Genomic profiling of Mycobacterium tuberculosis strains, Myanmar, comparing discriminatory power offered by GeneXpert (Cepheid,) and additional genotypic testing, such as line-probe assay or whole-genome sequencing..We compared the results of the GeneXpert, phenotypic DST, and genomic analyses to further evaluate drug resistance (- 1). Of 118 cases diagnosed as RS by using GeneXpert, 16 (14%) were identified as isoniazid resistant on the basis of genomic analyses (- 1); resistance was conferred either by a mutation in the katG gene (S315T; 12 [75%] of 16) or in the promoter region of the inhA gene (c-15t; 4 [25%] of 16) (Table 2; - 1). All 16 cases were phenotypically confirmed as isoniazid resistant .Prevalence of resistance-conferring mutations in genes of phenotypically resistant isolates of Mycobacterium tuberculosis strains, Myanmar. A) katG and inhA; B) embB; C) rpsL; D) gyrA; E) ethA and inhA; F) rrs; G) rpoB. . Prevalence of resistance-conferring mutations in genes of phenotypically resistant isolates of Mycobacterium tuberculosis strains, Myanmar. A) katG and inhA; B) embB; C) ...All 191 RR isolates identified by GeneXpert were phenotypically resistant; the S450L mutation in the rpoB gene was the dominant mutation (137 [72%] of 191 (Table 2; - 2). WGS further identified that 10 (5%) were only rifampin resistant (pre-MDR), 144 (75%) were MDR, 31 (16%) were pre-XDR, and 6 (3%) were XDR; results were confirmed by phenotypic DST (- 1). All pre-XDR isolates harbored mutations in the gyrA gene, and D94G was most prevalent (12 [39%] of 31), followed by A90V (8 [26%] of 31) (Table 2; - 2). Resistance to aminoglycoside injectable drugs (XDR) was predominantly associated with rrs A1401G (4 [6 [67%] of 6) and G1484T (2 [33%] of 6) mutations. Mutations in the embB gene (M306V; 42 [53%] of 80), the M306I mutant (34 [43%] of 80), and mutations in the rpsl gene (K43R; 126 [90%] of 140) were present in all ethambutol-resistant and streptomycin-resistant isolates, resulting in a sensitivity of 70.2% and a specificity of 79.5% for ethambutol and a sensitivity of 84.3% and a specificity of 55.9% for streptomycin (Table 2; - 2). Known mutations conferring resistance to new and repurposed drugs, such as bedaquiline, delamanid, pretomanid, linezolid and clofizamine, were not identified by WGS in the 207 drug-resistant isolates (26 pre-MDR, 144 MDR, 31 pre-XDR, 6 XDR). Maximum-likelihood tree based on whole-genome analysis of 309 Mycobacterium tuberculosis strains from Myanmar. Lineages and drug resistance status of isolates are shown. MDR indicates multidrug-resistant to 2 first-line drugs (isoniazid and rifampin); pre-MDR,