AnimalS-nitrosoglutathione reductase (GSNOR) governs the extent of cellularS-nitrosylation, a key redox-based posttranslational modification. Mutations inAtGSNOR1, anArabidopsis thaliana GSNOR, modulate the extent of cellularS-nitrosothiol (SNO) formation in this model plant species. Loss ofAtGSNOR1function increased SNO levels, disabling plant defense responses conferred by distinct resistance (R) gene subclasses. Furthermore, in the absence ofAtGSNOR1, both basal and nonhost disease resistance are also compromised. Conversely, increased AtGSNOR1 activity reduced SNO formation, enhancing protection against ordinarily virulent microbial pathogens. Here we demonstrate that AtGSNOR1 positively regulates the signaling network controlled by the plant immune system activator, salicylic acid. This contrasts with the function of this enzyme in mice during endotoxic shock, where GSNOR antagonizes inflammatory responses. Our data imply SNO formation and turnover regulate multiple modes of plant disease resistance.