Interestingly, compensatory mechanisms that limit Fyn hyperactivity have been also reported in mice model of AD, overexpressing hAPP, consisting in a significant increase in phosphatase STEP levels, which dephosphorylates and inactivates Fyn [13] and consequently, reduces NMDA receptor phosphorylation and internalization and prevent synaptic dysfunctions [13,182,221]. Here, FYN is linked to Alzheimer disease.