Rice employs sophisticated and multilayered regulatory networks to precisely modulate innate immune responses against diverse pathogens. Although post-transcriptional control has emerged as a vital layer of immune regulation, the mechanisms by which RNA-binding proteins (RBPs) govern rice immune responses remain largely unclear. Here, we report that the GYF-domain RBP MHZ9 acts as a negative regulator of rice disease resistance. MHZ9 directly binds to the mRNAs of the novel nucleotide-binding leucine-rich repeat receptor (NLR) genes and represses their translation, thus preventing excessive NLR accumulation. OsMAPK3/6, the core kinases in PTI signaling, physically interact with MHZ9 and specifically phosphorylate it at Ser50. This modification impairs the RNA-binding and translational repression activities of MHZ9, thus relieving inhibition of NLR translation upon pathogen infection. Conservation of the Ser50 residue across plant species but not in animals suggests that its phosphorylation is critical for plant immunity and likely plant-specific. Genetic analyses demonstrate that RP1 and RP5 are required for the enhanced blast resistance in mhz9, and Ser50 phosphorylation of MHZ9 serves as a critical switch to inactivate MHZ9 and activate immune responses. Our findings uncover a novel regulatory module where OsMAPK3-mediated MHZ9 Ser50 phosphorylation couples PTI signaling to post-transcriptional control of NLRs, shedding light on the molecular basis of immunity-growth balance in rice.