clonogens increased the likelihood that it will be able to withstand treatment with radiation. Secondly, the number of cells that are proliferat­ing and the tumor growth kinetics within the tumor can have an impact on response to EBRT. Rapidly dividing cells are typically more radio­sensitive because they are less likely to be able to repair DNA damage, are more likely to be in a radiosensitive portion of the cell cycle when receiving radiation, and are more likely to reas­sort into a radiosensitive portion of the cell cycle with fractionation of treatment [11, 12]. Additionally, increasing levels of hypoxia adversely impact the effect of EBRT.Since most of the radiation damage delivered by photons is mediated by oxygenated free radicals, the absence of oxygen limits the potency of radiation therapy, and tumors with poor circulation display increased radioresistance [13, 14]. Fourth, differ­ent tumor cells have a varying degree of ability to repair DNA damage, and this intrinsic ability to repair the DNA has a signicant impact on radio­sensitivity. In one study, investigators transfected the double-strand break repair gene DNA-PKcs into a cloned tumor cell line from severe com­bined immunodecient mice and then trans­planted this tumor in the same strain of mice and were able to show an increase in tumor cell radio­resistance by the introduction of DNA-PKcs, leading the authors to conclude that the intrinsic radiosensitivity of tumor cells is a major factor in determining radiosensitivity [15].