If, on the other hand, the second AD stage is driven not by iAβ but by another, yet unidentified, agent, assaying options would be limited to determining levels of the intact iAβ and to monitoring hyperphosphorylation of tau protein and the formation of NFTs; in any case, the potential therapeutic effects of the iAβ depletion treatment could be quantified. The gene discussed is MAPT; the disease is Alzheimer disease.