UDCA suppressed HCC growth in vivo in a dose- and time-dependent apoptosis fashion by upregulating the Bax to Bcl-2 ratio, Smac, Livin and caspase-3 expressions (Zhu et al., 2014; Liu et al., 2015), serving as a therapeutic candidate for HCC treatment. The gene discussed is BCL2; the disease is hepatocellular carcinoma.