We next tested the ability of H-1152 to antagonize elevated TEAD/YAP transcription in human tumors with endogenous lesions in Hippo pathway core components, NF2 and/or LATS1/2 (H2052, H2373, MSTO-211H mesotheliomas, MDA-MB-157 breast carcinoma and Snu387 hepatocellular carcinoma), YAP amplification (SF268 glioma) or both Hippo pathway and p53 DNA contact mutations (MDA-MB-231 breast carcinoma). The gene discussed is LATS1; the disease is central nervous system cancer.