For example, in alignment with the results demonstrating the association between decreased YAP levels and AD pathology, YAP knockdown in glial U251 cells expressing mutant APP increased levels of Aβ42 and tau phosphorylation, whereas YAP overexpression reduced these AD hallmarks, and also impacted proteins involved in Aβ generation and tau phosphorylation [20]. This evidence concerns the gene APP and Alzheimer disease.