The bounce‐back response is controlled by SKN‐1, which is a transcription factor that promotes resistance to proteotoxic stress, oxidative stress, as well as pathogen infection.[88, 89, 90] Overall, these findings in C. elegans suggest that proteasome blockade stimulates the activation of the IPR and the bounce‐back response as distinct, non‐overlapping stress/immune responses. Here, PRPS1 is linked to infection.