Recent studies have discovered that itaconate, besides its pro-inflammatory properties in bacterial infection and hypoxic settings, can exert anti-inflammatory effects in M1-like macrophages by limiting succinate oxidation, a critical step in the citric acid cycle, to inhibit mitochondria ROS production and downstream M1-like marker expression; itaconate can also induce cysteine alkylation and activate Nrf2 (nuclear factor erythroid 2-related factor 2), a sensor of oxidative stress, to suppress transcription of pro-inflammatory genes in macrophages [53, 135–137]. This evidence concerns the gene NFE2L2 and bacterial infectious disease.