For example, in BC, cell fate after radiation exposure depends on many factors such as hormone receptor status (estrogen and progesterone receptors, and human epidermal growth factor receptor 2), the number of tumor cancer stem cells present before initiation of RT and their ability to repopulate during the course of RT, effects of the tumor microenvironment such as hypoxia, stromal interaction and variations in the intrinsic sensitivity of cells to radiation, modulation of DNA repair or other cell survival pathways [5–8]. This evidence concerns the gene PGR and breast cancer.