In support of PP2A acting as a activator, the results showed that knockdown of PP2A catalytic subunits impaired the PP2A-induced dephosphorylation of its downstream responsive substrates like Bcl-2 at Ser 70 whereas overexpression of PP2A has the opposite results, which demonstrated that PP2A activation was involved in JS-K-induced apoptosis of sensitive HCC cells. Here, BCL2 is linked to hepatocellular carcinoma.