Given the above mechanism regarding the mutant Huntington gene, a slightly integrated pathway can be summarized in which both Mst1 activation and YAP phosphorylation attenuate the combination of YAP and TEAD via reducing the nuclear translocation of YAP, which all induce transcriptional interference, cytoskeletal disruption, protein mishandling, altered mitochondrial dynamics, and excitotoxicity and disordered calcium signaling to cause the Huntington gene mutation, like the CAG repeat that easily occurs in HD. The gene discussed is MST1; the disease is Huntington disease.