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Loss of YAP1/TAZ expression in the pancreatic endocrine compartment is not a passive consequence of endocrine specification, rather, Hippo pathway-mediated inhibition of YAP1/TAZ in endocrine progenitors is a prerequisite for endocrine specification and differentiation.

P-body is a new downstream effector of YAP/TAZ for tumorigenesis and tumor progression, suggesting disruption of P-bodies as a potential therapeutic strategy for tumors with active YAP.

Low expression of Cbfb may be the cause of osteoarthritis, and local admission of Cbfb may rescue and protect against osteoarthritis through decreasing Wnt/β-catenin signaling, and increasing Hippo/Yap signaling and Tgfβ/Smad2/3 signaling in osteoarthritis articular cartilage.

TEAD1 is a major partner transcription factor of YAP/TAZ crucial for developmental myelination and remyelination of peripheral nerves.

In response to disruption of barrier functions mediated by septate junctions, Drosophila epithelial cells restrict endosomal degradation of transmembrane cell adhesion proteins to promote their recycling in order to maintain tissue integrity.

Genetic analysis of Hippo pathway kinases in a close unicellular relative of animals suggests an ancestral role of this ancient pathway in regulating cytoskeletal dynamics and density of multicellular aggregates.