We found that RBM8A overexpression promoted proliferation, reduced apoptosis and increased the chemotherapeutic resistance of HCC cells to OXA, while RBM8A knockdown reversed these effects, consistent with reports that the deletion of the RBM8A gene down-regulates Bcl-Xs, Bim, and Mcl-1, as well as several proapoptotic genes, including members of the Bcl-2 family, thereby inducing apoptosis (24). The gene discussed is BCL2; the disease is hepatocellular carcinoma.