The high level of SA at the infection site promotes NPR3-mediated degradation of NPR1 (ref. 23) to remove its repression on ETI (PCD) and alleviate its crosstalk inhibition on JA signalling, meanwhile we propose that degradation of JAZs by NPR3 and NPR4 directly activates JA signalling, which is further amplified by de novo JA synthesis. Here, NPR3 is linked to infection.