LATS1 and neoplasm: We demonstrate that targeting dysregulated YAP/TAZ activity using a small molecule inhibitor of the TEAD transcription factors, which are key mediators of YAP/TAZ-regulated gene expression (Chan et al, 2009; Zhao et al, 2008), prevents the development of tumors driven by Lats1/2-deletion in the mammary epithelium, including blocking the onset of the tumor-stromal niche.