Furthermore, decreased KIBRA levels in AD could reduce LATS1/2 phosphorylation, leading to increased nuclear YAP levels, which could promote neurodegeneration through p73-mediated apoptosis or aberrant cell cycle re-entry through interaction with TEAD, though the link between decreased KIBRA levels and hypo-Hippo signaling has yet to be demonstrated in AD models. Here, YAP1 is linked to Alzheimer disease.