Since it was reported that SA induced UPR genes when exogenously administered to Arabidopsis [55] or during pathogen infection [56], and that the induction involved activation of the IRE1/bZIP60 and bZIP28 pathways [55], our data showing that UPR impairment hampered SA biosynthesis let us hypothesize the occurrence of a reciprocal regulatory pathway, in which proper UPR is necessary to increase SA levels, a fact that in turn enhances UPR, according to a positive feedback mechanism. This evidence concerns the gene ERN1 and infection.