The up-regulation of SA content and related genes (PAL, NPR1) in the early stage (12 hpi) treated with CX-3 and (R)-(-) -mellein (Figure 5a,b) might be a “pseudo-defense” response triggered by pathogenic bacteria, which antagonizes the subsequent JA-dependent defense by consuming SA synthesis precursors, similar to the strategy of viruses in tomatoes promoting infection by manipulating the SA-IAA balance [17]. The gene discussed is NPR1; the disease is infection.