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RseA is the critical central regulator of the σE-dependent stress response in E. coli and other related bacteria. The synthesis of RseA is controlled at the transcriptional level by several promoters and transcriptional regulators, including σE itself at two σE-dependent promoters: rpoEP and rseAP3. The presence of these two independent polycistrons encoding rseA is potentially redundant. We hypothesized that post-transcriptional control of the rseAP3 transcript was necessary to overcome this redundancy. However, to date, nothing is known about the post-transcriptional control of the rseAP3 transcript. We executed a targeted genetic screen to identify small RNA regulators of the rseAP3 transcript and identified RyhB and FnrS as small RNA activators of the RseA P3 transcript. Through genetic analysis, we confirmed that a direct interaction occurs between RyhB and RseA. We also identified sequences within the 5′ untranslated region (UTR) of RseA that were inhibitory for RseA expression. Point mutations predicted to prevent an interaction between RyhB and RseA resulted in increased RseA expression. Taken together, this suggests that the 5’ UTR of the RseAP3 transcript prevents optimal expression of RseA, preventing redundancy due to RseA expression from the σE-dependent rpoEP, and this is overcome by the stimulatory activity of RyhB and FnrS.