We previously reported that stress-activated p38K can phosphorylate Thr167 of Bax, leading to its translocation to mitochondria and initiation of mitochondria-dependent apoptosis when cultured hepatoma cells are exposed to cell death stimulants such as staurosporine, etoposide, and hydrogen peroxide, or UV exposure [16]. This evidence concerns the gene BAX and hepatocellular carcinoma.