β-Amyloid-induced cell death is attenuated in cortical neurons from JNJ3-null mice, and JNK3 mediates this cell death through the activation of c-Jun and the enhanced expression of Fas ligand, a protein that plays a role in programmed cell death (apoptosis) and has been implicated in the pathogenesis of Alzheimer’s disease (AD). This evidence concerns the gene FASLG and Alzheimer disease.