YAP1 and Alzheimer disease: Specifically, knockdown of LATS1/2 homolog wts-1 exacerbated abnormal lysosomal morphology in the AD model, while knockdown of YAP and TEAD homologs yap-1 and egl-44 attenuated morphological abnormality, reduced autophagosome accumulation, and rescued decreased expression of V-ATPase subunits necessary for lysosome acidification [25].