Our data suggest that cells have adapted the UPR pathway for a specific response to PFTs in order to promote cellular defense against this common form of pathogenic attack. First, we found that loss of the xbp-1 arm of the UPR does not lead to hypersensitivity to a heavy metal or hydrogen peroxide nor does loss of either xbp-1 or atf-6 lead to decreased protection against a bacterial pathogen that lacks a PFT. Second, the ire-1-xbp-1 and atf-6 arms of the UPR are involved in the defense but the pek-1 arm is not. Third, the activation and function of the UPR in PFT defenses can be separated from the role of the UPR in dealing with unfolded proteins (here tested using the drug tunicamycin) in two ways: 1) the relative importance of the various arms of the UPR for defense against PFT is different than their importance for protection against unfolded proteins and 2) the activation of the ire-1-xbp-1 pathway by PFT, but not unfolded proteins, requires p38 MAPK (see below).