Since induction of PTI genes causes ER stress (Wang et al., 2005; Moreno et al., 2012; Kørner et al., 2015), we propose that the Hpa-suppressed PTI during the early stages of infection is sufficient in BABA-primed cells to trigger moderate levels of ER stress and so allow for cytoplasmic translocation of IBI1, where it interacts with the ABA-induced pool of defense-regulatory VOZ1/2 TFs. This evidence concerns the gene HPSE and infection.