Microbes are often subjected to oxidative stress in nature that badly affects their growth rate and viability. Although the response of microbes against oxidative stress has been characterized at the chemical, physiological, and molecular levels, the mechanism of gene-regulation network adaptations of bacteria in response to oxidative stress remains largely unknown. In this study, transcriptomic profiling of glyphosate-tolerant Enterobacter strain NRS-1 was analyzed under 9 mM H2O2 stress using RNA-seq and qRT-PCR. The lag period in the growth of NRS-1 was very short compared with wild-type strain under H2O2 treatment. A total of 113 genes are identified as differentially expressed genes (DEGs) under H2O2 that include 38 upregulated and 75 downregulated transcripts. But not any genes regulated by major oxidative regulons, viz., oxyR, soxR, rpoS, perR, ohrR, and sigma(B), have been reported in DEGs, hence potentially reflecting that specific changes have occurred in NRS-1 for adaptation to oxidative stress. Based on the functions of the DEGs, six elements namely formate dehydrogenase, processes associated with iron ions, repair programs, multidrug resistance, antioxidant defense, and energy generation (mqo, sdhC) might have contributed for stress tolerance in NRS-1. These elements are proposed to form a molecular network explaining gene response of NRS-1 to stress, and ensure global cell protection and growth recovery of NRS-1. These findings enrich the view of gene regulation in bacteria in response to H2O2 oxidative stress.