Systemic Acquired Resistance (SAR) is a plant defense mechanism triggered by pathogen infection, leading to broad-spectrum resistance. It is activated after a necrotic lesion forms, either through hypersensitive response (HR) or disease symptoms. SAR involves the expression of SAR genes and is distinct from other resistance responses due to its broad pathogen protection and unique gene expression patterns. SAR can be induced by various pathogens, including viruses, bacteria, and fungi, and is characterized by the production of pathogenesis-related (PR) proteins, such as PR-1, PR-2, PR-3, PR-4, PR-5, and others. These proteins contribute to disease resistance by exhibiting antimicrobial activity and synergistic effects. Salicylic acid (SA) plays a crucial role in SAR signaling. SA accumulation is required for SAR induction, and its levels increase significantly after pathogen infection. SA is involved in the signaling cascade that leads to SAR, and its absence, as in the nahG transgenic plants, prevents SAR. However, SA is not the long-distance signal that translocates from the infection site to activate SAR elsewhere in the plant. Instead, SA is essential for SAR signal transduction and acts downstream of the long-distance signal. The biosynthesis of SA begins with the conversion of phenylalanine to trans-cinnamic acid (t-CA) by phenylalanine ammonia-lyase (PAL). t-CA is then converted to benzoic acid (BA), which is hydroxylated to SA. SA is involved in the signaling pathway that leads to SAR, and its accumulation is necessary for the induction of SAR genes and resistance. SA also plays a role in the oxidative burst, which is a key component of the plant's defense response. Chemical activators of SAR, such as 2,6-dichloroisonicotinic acid (INA) and benzothiadiazole (BTH), can induce SAR without pathogen infection. These chemicals induce the expression of SAR genes and enhance disease resistance. However, they do not directly act on the pathogen, and their effectiveness is dependent on SA signaling. Mutants of Arabidopsis have been identified that exhibit constitutive SAR or compromised SAR responses. These mutants provide insights into the SAR signal transduction pathway and the role of SA in disease resistance. The identification of SAR mutants has helped elucidate the steps involved in SAR signaling and the interactions between SA, cell death, and disease resistance. In conclusion, SAR is a critical plant defense mechanism that involves complex signaling pathways and the production of defense-related proteins. Understanding SAR is essential for developing strategies to enhance plant resistance to pathogens, both through genetic engineering and the use of chemical activators. Further research is needed to fully understand the mechanisms of SAR and its role in plant disease resistance.Systemic Acquired Resistance (SAR) is a plant defense mechanism triggered by pathogen infection, leading to broad-spectrum resistance. It is activated after a necrotic lesion forms, either through hypersensitive response (HR) or disease symptoms. SAR involves the expression of SAR genes and is distinct from other resistance responses due to its broad pathogen protection and unique gene expression patterns. SAR can be induced by various pathogens, including viruses, bacteria, and fungi, and is characterized by the production of pathogenesis-related (PR) proteins, such as PR-1, PR-2, PR-3, PR-4, PR-5, and others. These proteins contribute to disease resistance by exhibiting antimicrobial activity and synergistic effects. Salicylic acid (SA) plays a crucial role in SAR signaling. SA accumulation is required for SAR induction, and its levels increase significantly after pathogen infection. SA is involved in the signaling cascade that leads to SAR, and its absence, as in the nahG transgenic plants, prevents SAR. However, SA is not the long-distance signal that translocates from the infection site to activate SAR elsewhere in the plant. Instead, SA is essential for SAR signal transduction and acts downstream of the long-distance signal. The biosynthesis of SA begins with the conversion of phenylalanine to trans-cinnamic acid (t-CA) by phenylalanine ammonia-lyase (PAL). t-CA is then converted to benzoic acid (BA), which is hydroxylated to SA. SA is involved in the signaling pathway that leads to SAR, and its accumulation is necessary for the induction of SAR genes and resistance. SA also plays a role in the oxidative burst, which is a key component of the plant's defense response. Chemical activators of SAR, such as 2,6-dichloroisonicotinic acid (INA) and benzothiadiazole (BTH), can induce SAR without pathogen infection. These chemicals induce the expression of SAR genes and enhance disease resistance. However, they do not directly act on the pathogen, and their effectiveness is dependent on SA signaling. Mutants of Arabidopsis have been identified that exhibit constitutive SAR or compromised SAR responses. These mutants provide insights into the SAR signal transduction pathway and the role of SA in disease resistance. The identification of SAR mutants has helped elucidate the steps involved in SAR signaling and the interactions between SA, cell death, and disease resistance. In conclusion, SAR is a critical plant defense mechanism that involves complex signaling pathways and the production of defense-related proteins. Understanding SAR is essential for developing strategies to enhance plant resistance to pathogens, both through genetic engineering and the use of chemical activators. Further research is needed to fully understand the mechanisms of SAR and its role in plant disease resistance.