The study investigates the role of nitric oxide (NO) in the latency of *Mycobacterium tuberculosis* (Mtb). NO, produced by activated macrophages, is known to have antimycobacterial properties and can inhibit aerobic respiration. The researchers found that low, nontoxic concentrations of NO induce a 48-gene regulon via the response regulator DosR, which inhibits aerobic respiration and reversibly slows bacterial growth. This regulation is similar to that of hypoxia, suggesting a common mechanism of action. The dormancy regulon genes are essential for the survival of Mtb during prolonged periods of in vitro dormancy. The study also suggests that cytochrome c oxidase (CcO) may serve as a sensor for both NO and low O2 levels, integrating their signals to control Mtb's physiological state. The findings provide insights into how NO produced by the immune system limits Mtb growth and contributes to the latency of tuberculosis.The study investigates the role of nitric oxide (NO) in the latency of *Mycobacterium tuberculosis* (Mtb). NO, produced by activated macrophages, is known to have antimycobacterial properties and can inhibit aerobic respiration. The researchers found that low, nontoxic concentrations of NO induce a 48-gene regulon via the response regulator DosR, which inhibits aerobic respiration and reversibly slows bacterial growth. This regulation is similar to that of hypoxia, suggesting a common mechanism of action. The dormancy regulon genes are essential for the survival of Mtb during prolonged periods of in vitro dormancy. The study also suggests that cytochrome c oxidase (CcO) may serve as a sensor for both NO and low O2 levels, integrating their signals to control Mtb's physiological state. The findings provide insights into how NO produced by the immune system limits Mtb growth and contributes to the latency of tuberculosis.