Although cell cycle arrest enhances the radiosensitization of malignancies through the promotion of apoptosis [34, 35], owing to the relatively weak inhibitory effect of ITGB3-KD on the G1 phase, we hypothesize that a more pivotal mechanism is involved in facilitating the radiosensitization of osteosarcoma cells, potentially by promoting apoptosis and other biological processes. Here, ITGB3 is linked to osteosarcoma.