The upregulation of endogenous Trx1 and Trx2 expression and the administration of exogenous Trx1 inducers can confer neuroprotective effects against AD through the activation of prosurvival pathways (PI3K/Akt and ERK pathways) and the suppression of oxidative stress, inflammation (TXNIP, NLRP3, and NF-κB), and apoptosis (ASK1/JNK/p38 MAPK and the caspase-1 and -12 pathways) [78]. The gene discussed is AKT1; the disease is Alzheimer disease.