The ER stress response has been previously associated with pathogenic attack, mostly in the opposite direction shown here, e.g., aiding viral replication and pathogenesis ( [21] and references therein). In a few cases, the ER stress response has been linked with innate immunity since induction of ER stress can activate CREB-H, which in turn promotes the acute inflammatory response [22] . It has also been suggested that IRE-1 could influence immunity via its association with TRAF-2, which in turn can regulate NF-kB [23] . Data from studies in plants suggest that in response to pathogens, signals can be produced that lead to an ''anticipatory'' UPR to handle the massive synthesis of new secretory proteins required [24] .