Plant Resistance Inducers (PRIs) can elicit the plant immune system and serve as a lever to reduce the use of pesticides. Under controlled conditions, PRIs may significantly control pests, but in the field, their efficiency is much more uncertain. Indeed, the efficiency of plant immune system elicitation highly depends on the plant's physiological status. Nitrogen is one of the most important nutrients for plant growth and is widely used in agricultural production. While the effect of nitrogen limitation on disease susceptibility is inconsistent according to plant species and pathogens, several studies have shown that plant nitrogen limitation induces secondary metabolic pathways also involved in biotic stress responses, such as the phenylpropanoids biosynthesis pathway. In this context, this study focuses on the effect of the combination of low nitrogen status and acibenzolar-S-methyl (ASM) treatments on apple plants (Malus domestica). ASM is a salicylic acid analog and, therefore, induces numerous plant defense responses. Our research hypothesis is that nitrogen limitation could improve ASM efficiency against two phytopathogenic microorganisms, bacteria Erwinia amylovora (fire blight), and fungi Venturia inaequalis (apple scab), by an increased, diversified, and/or persistent plant response to stimulation. To test this hypothesis, apple seedlings were grown in greenhouses under contrasting N regimes obtained by sub-irrigation with continuous sufficient nitrate fertilization or transient limitation. Plants were then treated or not with ASM 48h before N resupply or 24h after. Two days after treatment, young leaves were inoculated with Erwinia amylovora or Venturia inaequalis, and disease symptoms were recorded. Results show a clear relationship between plant nitrogen status and ASM efficiency, with N-limited plants treated with ASM exhibiting a 2 or 3-fold higher level of protection than the control plants against fire blight or apple scab, respectively. The relative expression level of 29 well-known defense genes usually responding to ASM treatment (qPCR analysis) could not explain these differences. Therefore, transcriptomic and metabolomic (primary and secondary metabolites) analyses have been undertaken to explain the strong protection phenotype obtained for ASM x N-limited plants. Omics results will be presented and discussed regarding the different ASM-protection phenotypes observed.