In AD, it has been observed that hyperphosphorylations in Tau by proline-directed kinases such as glycogen synthase kinase-3 beta (GSK-3β) and cyclin dependent kinase 5 (CDK5) kinases induce Tau self-assembly in NFT [1], which prevents Tau binding to microtubules, leading to synaptic dysfunction [22] and its deposition in the form of NFTs, resulting in the formation of aggregates in the brainstem nuclei [22]. The gene discussed is CDK5; the disease is Alzheimer disease.