591 Additionally, another Keap1-Nrf2 PPI inhibitor 74, which combined conformational features significantly similar to the Keap1-Nrf2 ETGE complex, revealed the unique inhibition mechanism and provided an innovative strategy for the development of new Keap1-Nrf2 PPI inhibitors.592 In summary, inhibition or activation of fundamental pathological interactions presents an alternative therapeutic avenue for AD. This evidence concerns the gene KEAP1 and Alzheimer disease.