Decreased coxsackie and adenovirus receptor (CAR) expression was correlated with increased tumorigenicity and metastasis formation in the LNCaP-derived human prostate cancer subline C4-2B, however, both aforementioned HDAC inhibitors restored CAR surface expression and augmented TRAIL-mediated caspase activity based on enhanced adenoviral transduction efficacy when combined with TRAIL gene therapy[70]. The gene discussed is HDAC9; the disease is prostate carcinoma.