These include the induction of endogenous SA in response to pathogen infection, the perception of SA by SA receptors (Nonexpressor of Pathogenesis Related Protein 3 (NPR3) and NPR4), the release of NPR1 monomers and translocation in nucleus as well as the interaction of nuclear NPR1 and TGACG sequence-specific binding protein (TGA) transcription factors, and the activation of PRs58, 59, 60, 69, 70. This evidence concerns the gene NPR1 and infection.