Considering the activation of NRF2 via inhibition of the KEAP1‐NRF2 interaction has been found to be neuroprotective in a cellular PD model,[61] the regulation of cellular redox homeostasis and mitochondrial function by NRF2 presents a possible therapeutic target in PD and other neurodegenerative diseases associated with p62 deregulation. Here, KEAP1 is linked to Parkinson disease.