Increased abundance of this endogenous inhibitor of cysteine cathepsins could modulate key aspects of neurobiology by the inhibition of the activity of cathepsin B. This may be particularly relevant in AD pathogenesis in which abundance and activity of the enzyme is upregulated and has been suggested to impact on a number of key disease mechanisms, including APP processing, amyloid-β catabolism, and the neuroinflammatory response to pathology; particularly via the activation of inflammasomes [35–37]. The gene discussed is APP; the disease is Alzheimer disease.