Tsai et al. reported that inhibiting histone deacetylase 4 (HDAC4) using synthetic pan-HDAC inhibitor panobinostat or short hairpin RNAs could inhibit the HR activity in RT-treated HCC cells via impairing the DNA repair function of Rad51 to incur persistent DNA damage, leading to pronounced synthetic lethality that significantly promoted apoptosis of HCC cells after radiotherapy 132. This evidence concerns the gene RAD51 and hepatocellular carcinoma.