The study investigates the role of nitric oxide (NO) and S-nitrosylation in plant immune signaling. Upon recognition of pathogen/microbial-associated molecular patterns (P/MAMPs), such as flagellin (flg22) and elongation factor Tu (efl18), plant cell surface receptors like FLS2 and EFR trigger a rapid nitrosative burst, leading to the accumulation of NO. This NO accumulation results in the S-nitrosylation of the receptor-like cytoplasmic kinase (RLCK), botrytis-induced kinase 1 (BIK1) at Cys80, promoting its phosphorylation and activation. S-nitrosylation also increases BIK1's interaction with RBOHD, the source of apoplastic reactive oxygen species (ROS), enhancing ROS production. The study demonstrates that NO is a key regulator of ROS production during P/MAMP-triggered immunity (PTI) and that BIK1 Cys80-SNO formation is crucial for PTI signaling and plant immunity.The study investigates the role of nitric oxide (NO) and S-nitrosylation in plant immune signaling. Upon recognition of pathogen/microbial-associated molecular patterns (P/MAMPs), such as flagellin (flg22) and elongation factor Tu (efl18), plant cell surface receptors like FLS2 and EFR trigger a rapid nitrosative burst, leading to the accumulation of NO. This NO accumulation results in the S-nitrosylation of the receptor-like cytoplasmic kinase (RLCK), botrytis-induced kinase 1 (BIK1) at Cys80, promoting its phosphorylation and activation. S-nitrosylation also increases BIK1's interaction with RBOHD, the source of apoplastic reactive oxygen species (ROS), enhancing ROS production. The study demonstrates that NO is a key regulator of ROS production during P/MAMP-triggered immunity (PTI) and that BIK1 Cys80-SNO formation is crucial for PTI signaling and plant immunity.