In a past in vitro study by Liu and colleagues [62], evidence was provided suggesting STAT3 may play a role in AD pathophysiology via its role in regulating expression levels of BACE1 and the catalytic subunit of γ-secretase, presenilin-1—molecules with well-characterized roles in catalyzing APP cleavage into Aβ fragments and promoting amyloid deposition. Here, APP is linked to Alzheimer disease.