Multiple lines of evidence support a key role for TEADs in this context: (1) mutating the TEAD-binding site in YAP or TAZ completely blocks their anti-cancer activity in multiple YAPoff solid cancers [14, 24, 30], (2) knockout of TEADs abrogates, while overexpression of TEADs enhances, YAP-driven cytostasis in SCLC [14], and (3) a TEAD DNA-binding domain fused to a VP64 transcriptional activation domain, which mimics YAP/TEAD activity [28,52], phenocopies the effects of ectopic YAP in YAPoff cancers [14]. Here, YAP1 is linked to small cell lung carcinoma.