Several chromatin immunoprecipitation (ChIP) studies reveal that TEADs serve as the primary effectors of the YAP/TAZ signaling: (1) 78% of the TEAD4-bound promoters and enhancers are co-occupied by YAP/TAZ in NF2-null breast cancer cell line MDA-MB-231 [14]; (2) YAP and TEAD1 co-occupy >80% of the promoters in MCF10A breast cancer cells [15]; and (3) 86% of all the YAP1 peaks contain at least one TEAD-binding site in SF268 glioblastoma cell line [16]. This evidence concerns the gene TEAD1 and breast carcinoma.