Once considered an environmental pollutant and toxic gas, nitric oxide (NO) has gained recognition for its key roles in mammalian physiology. At high (micromolar) concentrations, NO is used as an immune defense agent to kill invading pathogens. However, certain pathogens have evolved a mechanism to circumvent the mammalian immune response by expressing Flavodiiron Nitric Oxide Reductase (FNORs) that destroy NO, countering NO toxicity and facilitating microbial pathogenesis. Our group has been investigating how these FNORs detoxify NO by reduction to less toxic N2O, which is crucial for addressing the proliferation of these immune-resistant pathogens. The most logical intermediate in the N—N coupling reaction between two NO units is hyponitrite (ONNO2-); however, this intermediate has escaped experimental observations thus far. Understanding the binding modes of this intermediate as it is paramount to discerning how N—N coupling and N2O generation occur in FNORs. Recently, we reported the reactivity of two non-heme iron complexes with preformed hyponitrite.1 We found that the Lewis-acidity of the Fe-centers plays a key role in modulating the stability of Fe-hyponitrite species and were able to obtain a stable tetranuclear Fe-hyponitrite complex. Currently, we have been working on developing diiron hyponitrite complexes that better mimic the FNOR active site. Insights into hyponitrite reactivity at diiron FNOR model complexes will be discussed.