In addition to reducing Aβ42 and plaque levels in APP/PS1 mice, Figure 3A shows that PADK’s induction of active CatB is also linked to increased clearance of the β-secretase-derived carboxyterminal fragment of APP (APP-βCTF), an amyloidogenic species shown to accumulate in CatB- and LAMP1-positive organelles in the triple-transgenic (3×Tg) LaFerla mouse model of AD [35]. The gene discussed is TYRP1; the disease is Alzheimer disease.