Interestingly, some studies have shown that pathophysiological features of AD can be remedied by modulating NRG1/ErbB4 signaling; treatment of NRG1 in APP/PS1 transgenic mice inhibits neuronal apoptosis in APP/PS1 transgenic mice via ErbB4-dependent PI3-kinase/Akt pathway activation49, and also prevents soluble Aβ1-42-induced LTP impairment via ErbB4 activation50. The gene discussed is APP; the disease is Alzheimer disease.