Abstract: Radiotherapy is an essential part of cancer treatment, which leads to DNA double strains break. Homogeneous recombination and heterogeneous end conjunction are the main ways which can repair DNA double strains break in the cells. It is a novel strategy, which as recognize as the mechanism of damage to DNA strains, that radiosensitivity is enhanced by histone deacetylase(HDAC)inhibitor. HDAC inhibitor is able to antagonize specifically or nonspecifically HDAC whom is forming as four various sorts, as a consequence enhancing level of histone deacetylase, decoilization of chromosome and alternation on molecular structure of nucleolus. Firstly DNA is simply influenced by radioactivity due to HDAC inhibitor, and then HDAC inhibitor effects on decline activity of E2F1 transcript factors, which cause directly expressional inhibition on the repair proteins including Ku80, Rad51, thus the molecules are unable to recruited and polymerized into correspond protein compound, as a result of HDAC inhibitor the function of homogeneous recombination and heterogeneous end conjunction becomes minimized. As the circumstances are shown involving augment or non-augment of apoptosis among cancer cells, HDAC inhibitor enhance the radiosensitivity eventually, which has been applicated into clinical trials and obtain primary achievement.