Based on these data, we predicted that animals mutant in the p38 pathway should be more sensitive to PFT than animals mutant in the UPR pathway. This hypothesis is based on the fact that the p38 pathway is upstream of the UPR, is required for full activation of the UPR in response to PFT, and is involved in UPRindependent PFT defense pathways (e.g., ttm-2). Comparison of sek-1(km4) and xbp-1(zc12) mutant animals on Cry5B indicates sek-1(km4) animals are more severely intoxicated than xbp-1(zc12) animals at the same dose of Cry5B ( Figure 5G ). This conclusion was quantitatively confirmed by performing LC 50 experiments on N2 and sek-1(km4) animals (Table 1) . Whereas the LC 50 of xbp-1(zc12) animals on Cry5B is 5.8 fold lower than N2, the LC 50 of sek-1(km4) animals on Cry5B is 170 fold lower than N2.