Collectively, these results imply sensitivity of MLS, SySa and MPNST to pharmacologic inhibition of nuclear YAP1/TAZ-TEAD transcriptional activity in vitro, supporting the idea that dependency on YAP1/TAZ-TEAD signaling may provide a new target for therapeutic intervention in sarcoma patients with nuclear YAP1/TAZ activity. Here, HCCS is linked to sarcoma.