Based on recent findings, which pinpoint the pathogenic role of the pro NGF-p75NTR/sortilin pathway in AD neurodegeneration, it may be predicted that a prevailing Pro-NGF signaling system in absence of TrkA [51,52,53] will increase JNK activity, APPpT668 levels, impair APP–TrkA interaction, and generate Aβ. The gene discussed is NGF; the disease is Alzheimer disease.