The Aβ42 oligomers in cerebral plaques in AD activate the calmodulin-dependent protein kinase kinase CAMKK2-AMPK kinase pathway through phosphorylation of tau protein, and subsequent hyper-activation of CAMKK2 or AMPK by Aβ produces loss of dendritic spines in hippocampal neurons of transgenic mice for human Aβ precursor protein (Mairet-Coello et al., 2013). The gene discussed is CAMKK2; the disease is Alzheimer disease.