Clinical aspects of radiation oncology have been illuminated in this book in a sophisticated and comprehensive way. The development of double strand breaks of DNA is supposed to be given by radiation's technique of operation. Double strand breaks get mended by non-homologous end joining due to the acetylation of histone proteins by histone acetyltransferases (HATs). This repair can prove to be of beneficial function for radiation sensitization in clinical practice. The transcription and translation of a set of genes is being restrained by a tumor suppressor gene i.e. P53; and its metamorphosis has been involved in 60% of human cancers. The oscillation of DNA double strand break era and their interdependence on P53 status, ATM and ARF incitement have been calculated and designed for understanding the capability of this discovery.