We have focused on NO following the discovery by Kairui Mao et al.[19] of the role of NO generated from iNOS in the regulation of the NLRP3 inflammasome and a subsequent report suggesting the regulation of tuberculosis immunopathology by NO through the inhibition of NLRP3 inflammasome-dependent IL-1β processing[20]. The gene discussed is NLRP3; the disease is tuberculosis.