Necrotrophic fungi such as Botrytis cinerea and Alternaria brassicicola kill host plant cells to feed themselves on dead plant tissues. B. cinerea is responsible for the development of grey mould, while A. brassicicola triggers black spot disease, both contributing to significant agricultural losses worldwide. In this article, we have investigated the contribution of the Unfolded Protein Response (UPR) pathway in the resistance of the model plant Arabidopsis thaliana to these two fungi. This cellular signalling pathway serves as a cellular protective mechanism, enhancing the protein folding capacity of the endoplasmic reticulum (ER). It is activated in response to the accumulation of unfolded or misfolded proteins within the ER. Our data indicate that the main branch of the UPR, regulated by the proteins IRE1A and IRE1B, along with the transcription factor bZIP60, contribute to plant resistance to B. cinerea and A. brassicicola. The mutants ire1a/ire1b and bzip60 are indeed more susceptible to both pathogens. It correlates with the accumulation of mRNAs coding active bZIP60 in response to B. cinerea. Futhermore, the ER Quality Control (ER-QC) system is transcriptionally activated in response to B. cinerea, and mutation in the genes coding two of its component, the co-chaperone proteins SDF2 and ERdj3B, result in increased susceptibility to Botrytis. Proteins that are misfolded or aberrant can be targeted for proteasomal degradation through the ER-associated degradation (ERAD) pathway, assisted by the AAA+-ATPase CDC48. We showed that mutants in the genes coding the three arabidopsis CDC48 isoforms are more resistant to B. cinerea. To understand the involvement of IRE1 proteins and bZIP60 in immunity against B. cinerea, we adopted an RT-qPCR approach. Our data indicate that neither the classical defence genes typically induced by B. cinerea (PR1, PDF1.2, ORA59, PAD3) nor the genes responsible for ER-induced cell death (NAC089, Cathepsin B1, B2 and B3) are regulated by the IRE1A/bZIP60 pathway. However, we have demonstrated that mRNA coding the NAC053/NTL4 transcription factor accumulates significantly in the bzip60 mutant, in contrast to its closest homolog, NAC078/NTL11. Finally, both mutants nac053 and nac078 were more resistant to B. cinerea infection indicating that these transcription factors act as negative regulator of Arabidopsis defence against B. cinerea.