Systemic acquired resistance (SAR) is a distinct signal transduction pathway that enables plants to defend themselves against pathogens. After the formation of a necrotic lesion, either as part of the hypersensitive response (HR) or as a symptom of disease, the SAR pathway is activated, leading to broad-spectrum, systemic resistance. SAR can be distinguished from other disease resistance responses by its spectrum of pathogen protection and associated gene expression changes. In tobacco, SAR activation results in significant reduction of disease symptoms caused by various pathogens, but it is not effective against all pathogens. The expression of specific genes, known as SAR genes, is associated with SAR, and these genes are differentially expressed in response to different pathogens. The SAR signal transduction pathway functions as a potentiator or modulator of other disease resistance mechanisms, converting compatible plant-pathogen interactions into incompatible ones. Salicylic acid (SA) plays a crucial role in both SAR signaling and disease resistance. SA accumulation is required for SAR induction, and exogenous SA can induce SAR and SAR gene expression. However, SA is not likely to be the long-distance signal that triggers SAR in distal plant organs. Instead, SA acts as an essential signal downstream of the long-distance signal. The biosynthesis of SA involves the conversion of phenylalanine to trans-cinnamic acid by polyphenol oxidase (PAL), followed by the production of benzoic acid and subsequent hydroxylation to form SA. SA can be conjugated to glucose, and regulation of SA levels through conjugation may be important. Chemical activators of SAR, such as 2,6-dichloroisocoumarin (INA) and benzothiadiazole (BTH), have been identified. These chemicals induce SAR and provide broad-spectrum disease resistance in various crops. In contrast, mutants that are constitutively activated for SAR or compromised in their ability to launch the SAR response have been identified, providing insights into the steps in the SAR signal transduction pathway. For example, the lesion mimic mutants (lsd1 to lsd7 and acd2) exhibit spontaneous cell death and elevated SAR gene expression, while the constitutive immunity mutants (cim3) lack spontaneous cell death but exhibit constitutive SAR gene expression. In conclusion, the SAR signal transduction pathway is central to plant disease resistance. Understanding this pathway is important for both practical and theoretical reasons, as it provides a basis for developing genetically engineered plants with enhanced disease resistance or novel plant protection chemicals.Systemic acquired resistance (SAR) is a distinct signal transduction pathway that enables plants to defend themselves against pathogens. After the formation of a necrotic lesion, either as part of the hypersensitive response (HR) or as a symptom of disease, the SAR pathway is activated, leading to broad-spectrum, systemic resistance. SAR can be distinguished from other disease resistance responses by its spectrum of pathogen protection and associated gene expression changes. In tobacco, SAR activation results in significant reduction of disease symptoms caused by various pathogens, but it is not effective against all pathogens. The expression of specific genes, known as SAR genes, is associated with SAR, and these genes are differentially expressed in response to different pathogens. The SAR signal transduction pathway functions as a potentiator or modulator of other disease resistance mechanisms, converting compatible plant-pathogen interactions into incompatible ones. Salicylic acid (SA) plays a crucial role in both SAR signaling and disease resistance. SA accumulation is required for SAR induction, and exogenous SA can induce SAR and SAR gene expression. However, SA is not likely to be the long-distance signal that triggers SAR in distal plant organs. Instead, SA acts as an essential signal downstream of the long-distance signal. The biosynthesis of SA involves the conversion of phenylalanine to trans-cinnamic acid by polyphenol oxidase (PAL), followed by the production of benzoic acid and subsequent hydroxylation to form SA. SA can be conjugated to glucose, and regulation of SA levels through conjugation may be important. Chemical activators of SAR, such as 2,6-dichloroisocoumarin (INA) and benzothiadiazole (BTH), have been identified. These chemicals induce SAR and provide broad-spectrum disease resistance in various crops. In contrast, mutants that are constitutively activated for SAR or compromised in their ability to launch the SAR response have been identified, providing insights into the steps in the SAR signal transduction pathway. For example, the lesion mimic mutants (lsd1 to lsd7 and acd2) exhibit spontaneous cell death and elevated SAR gene expression, while the constitutive immunity mutants (cim3) lack spontaneous cell death but exhibit constitutive SAR gene expression. In conclusion, the SAR signal transduction pathway is central to plant disease resistance. Understanding this pathway is important for both practical and theoretical reasons, as it provides a basis for developing genetically engineered plants with enhanced disease resistance or novel plant protection chemicals.