Systemic acquired resistance (SAR) occurs when primary infected leaves produce several SAR-inducing chemical or mobile signals that are transported to uninfected distal parts via apoplastic or symplastic compartments and activate systemic immunity. The transport route of many chemicals associated with SAR is unknown. Recently, it was demonstrated that pathogen-infected cells preferentially transport salicylic acid (SA) through the apoplasts to uninfected areas. The pH gradient and deprotonation of SA may lead to apoplastic accumulation of SA before it accumulates in the cytosol following pathogen infection. Additionally, SA mobility over a long distance is essential for SAR, and transpiration controls the partitioning of SA into apoplasts and cuticles. On the other hand, glycerol-3-phosphate (G3P) and azelaic acid (AzA) travel via the plasmodesmata (PD) channel in the symplastic route. In this review, we discuss the role of SA as a mobile signal and the regulation of SA transport in SAR.