Synaptic localization of Fyn has been shown to worsen the phenotype in models of β-amyloidosis; however, it has also been reported that, despite total levels of Fyn are unchanged between human AD and control, in AD brains Fyn levels are increased in somas, where it colocalizes with tau tangles, and are decreased in synaptic compartments (Ho et al., 2005), suggesting a physiologic role of Fyn at synapses. The gene discussed is FYN; the disease is Alzheimer disease.