This is supported by findings in the J20 mice (a transgenic model overexpressing human APP with familial AD mutations), that reducing the Aβ-mediated activation of stress-related kinases p38 including MAPK, and c-Jun N-terminal kinase (JNK), inhibits early synaptic dysfunction in layer II of the EC (Criscuolo et al., 2017). The gene discussed is APP; the disease is Alzheimer disease.