Given that BTZ is potently cytotoxic in cultured Onc-p53 NSCLC cells but seems of limited efficacy as a single agent in unselected patients in clinical trials (12), we hypothesized that a combination of BTZ with an agent that abrogates prosurvival signaling, such as a BH3-mimetic (54, 55), would enhance BTZ efficacy. The gene discussed is CASC3; the disease is non-small cell lung carcinoma.