During inflammation and infection, Irg1/Itaconate pathway has been shown to control myeloid cell function through multiple mechanisms, such as succinate dehydrogenase (SDH) inhibition, nuclear factor erythroid 2-like 2 (NFE2L2 or NRF2) activation, and modulation of oxidative stress [20,22]. The gene discussed is NFE2L2; the disease is infection.