Systemic acquired resistance (SAR) is a form of broad-spectrum resistance induced in response to local infections that protects uninfected parts against subsequent secondary infections. SAR signaling requires two parallel branches, one regulated by salicylic acid (SA), and the other by pipecolic acid (Pip), azelaic acid (AzA) and glycerol-3-phosphate (G3P). AzA and G3P function downstream of the free radicals nitric oxide (NO) and reactive oxygen species (ROS). Normal induction of SAR also requires an intact cuticle, a waxy hydrophobic layer often considered a passive barrier from the environment. Detailed characterization of cuticle mutants showed that defective SAR in these was associated with reduced apoplastic transport of SA from local to distal tissues. The cuticle mutants showed normal symplastic transport of G3P and plasmodesmata permeability. Our results demonstrate that that transport of SA from local to distal tissues is important for SAR. Factors regulating SA transport will be discussed.