Inessence, the promoter region of the BACE1 genehosts binding sites for the redox-sensitive AP-1 and NF-κB; the activation ofwhich in an environment of chronic oxidative stress explains the enhancedtranscription of BACE1 [198], elevated JNK signalling [16], increased expression of BACE1 and increased PS1 activity, which have beendetected in AD brains [199–201]. The gene discussed is NFKB1; the disease is Alzheimer disease.