For over 60 years, salicylic acid (SA) has been known as a plant immune signal required for both basal and systemic acquired resistance (SAR). SA activates these immune responses by reprogramming up to 20% of the transcriptome through the function of NPR1. However, components in the NPR1-signaling hub, which appears as nuclear condensates, and the cascade of the NPR1-signaling pathway remained elusive due to difficulties in studying transcriptional cofactors whose chromosomal associations are often indirect and transient. To overcome this challenge, we applied TurboID to divulge the NPR1-proxiome, which detected key known NPR1-interactors and many new components of transcription-related complexes.