Reducing tau hyperphosphorylation by blocking protein kinases, such as GSK‐3β, CDK5, and c‐Jun N‐terminal kinases (JNK) is one alternative to treating AD, as their levels have been found to increase in AD brains.[43, 44, 45] Additionally, studies have shown that the downregulation of PP2A can lead to AD‐like pathology, including tau hyperphosphorylation and destabilization of microtubules.[46] As such, activating this phosphatase is another strategy against AD.[47]. This evidence concerns the gene GSK3B and Alzheimer disease.