A HDAC inhibitor quisinostat (JNJ-26481585) treatment significantly induced G0/G1 cell cycle arrest in the HCC cell line with a dose dependent increase in phosphorylation of JNK and c-Jun; furthermore, combination treatment using quisinostat and sorafenib markedly reduced JNK phosphorylation and induced apoptosis, suggesting that combination therapy could be useful in recovering patients from the burden of hepatocellular carcinoma [72]. The gene discussed is JUN; the disease is hepatocellular carcinoma.