Inhibition of HO‐1/BVR‐A pathway leads to the inability of its neuroprotective function, which is conducive to AD pathology progression in DS individuals.[359, 360] Treatment with Caffeic Acid Phenethyl Ester (CAPE) and its synthetic analog VP961, known for their ability to modulate NRF2 activity and facilitate NRF2 nuclear translocation, leading to enhanced antioxidant response in Ts2Cje mice (a Down syndrome mouse model) and human Down syndrome lymphoblastoid cell lines (LCLs).[362] Hence, targeting BACH1 and oxidative stress pathways could provide therapeutic strategies for the patients. This evidence concerns the gene BACH1 and Alzheimer disease.