The mechanistic target of rapamycin complex 2 (mTORC2) plays a critical role in tumor biology; however, its biological function in DNA damage repair remains poorly understood. To investigate its role, we established renal cancer cell lines with stable knockdown of Rictor, a core component of mTORC2, and subjected them to ionizing radiation. Subsequently, we performed a global phosphoproteomic analysis to profile phosphorylation events regulated by Rictor under radiation-induced stress.