Primary metabolism is essential for plant growth and development while its function in plant immunity is just emerging. Here we utilized genetics, molecular biology, transcriptomics and metabolomics to characterize the role of a gene SMO3 (suppressor of mos1 bon1, 3) coding for a glycolytic enzyme in plant immunity. From a genetic screen, we identified the SMO3 gene as a negative regulator of plant defense. The smo3 mutant is more resistant to a virulent pathogen Pseudomonas syringae pv. tomato DC3000 and has increased salicylic acid accumulation compared to wild type plant. Transcriptomic analyses showed that many immune responsive genes including one quarter of intracellular immune receptor NLR genes are up-regulated while genes involved in metabolic processes such as glycolysis are down-regulated in the mutant. Knocking out of SNC1 (suppressor of npr1-1, constitutive 1), one of the up-regulated NLR genes in the mutant, partially suppresses the elevated immunity of the mutant. These data indicate that NLR-mediated immune signaling is essential for the elevated immunity in the mutant. The SMO3 gene is predicted to encode two proteins with the short isoform functioning as a transcriptional repressor while the long isoform serving as a canonical glycolytic enzyme. Complementation test showed that only the long isoform could rescue the smo3 mutant defects, suggesting that its enzymatic function is critical for its role in immunity. A GC-MS analysis targeting primary metabolites revealed a significant increase of primary metabolites such as glucose in the mutant compared to wild type plant. This study indicates a significant impact of primary metabolism on plant immunity. Future research work will further explore how the enzymatic activity of SMO3 contributes to NLR gene expression and immune responses, which will provide a new insight into the impact of primary metabolism on growth and defense.