Notably, addition of okadaic acid (OA), a PP2A inhibitor, not only significantly abolished the effects of JS-K on the PP2A-C activation and the substrates of PP2A dephosphorylation, but also obviously protected against JS-K-induced apoptosis, such as Bax/Bcl-2 modulation and caspase successively activation in sensitive HCC cells. This evidence concerns the gene BAX and hepatocellular carcinoma.