Recent findings suggest that HCQ inactivates STAT3 [11] while prior work in transgenic AD mouse models has implicated enhanced STAT3 signaling in Aβ-induced neuronal death, reactive astrogliosis, impaired microglial clearance of Aβ as well as in cognitive impairment [49, 50], suggesting that inhibition of STAT3 signaling may target multiple molecular abnormalities and hence present a novel therapeutic approach in AD. The gene discussed is STAT3; the disease is Alzheimer disease.