The expression of CyclinD1 were downregulated and that of P53 were upregulated when HepG2 cells were treated with SBP-2A is the fingings confirmed that the combination of wild-type P53 and antisense CyclinD1 in HepG2 cells could improve the ability of SBP to induce tumour cell apoptosis and block the DNA synthesis cycle in the G0/G1 phase, this is mainly achieved by downregulating the protein expression of CDK and upregulating the Bax/Bcl-2 ratio. Here, BCL2 is linked to neoplasm.