Previously, we reported a novel etiopathogenic mechanism of AD in which the generation of I2CTF by the cleavage of I2PP2A/SET initiates a cascade of events, a key feature of which is the inhibition of PP2A activity and resulting AD-like pathologic alterations, including hyperphosphorylation of tau, β-amyloidosis, neurodegeneration and learning and memory impairment [22]. The gene discussed is MAPT; the disease is Alzheimer disease.