Our knowledge of the mechanistic basis of the strong link between IR and carcinogenesis has been based on early studies using various animal models and it is concluded that radiation tumorigenesis proceeds in a conventional multi-step mode following radiation-induced key gene losses from single-target cells (including possible stem cells) . These genes can be DNA damage response, apoptotic and cell cycle control genes and others. This radiation-induced GI can be transmitted over many generations after irradiation via the progeny of surviving cells . Complex DNA damage and the consequent less precise and/or delayed DNA repair certainly hold a pivotal role(s) in this association between IR and cancer . Last but not least, in order to draw the current picture of the factors contributing to radiation-induced carcinogenesis one should also add the non-targeted effects and the release of clastogenic factors in non-irradiated cells and tissues , as well as the involvement of inflammation and constant triggering of the immune system .