Typically, considering that the regulatory networks of senescence and stemness are largely overlapped with shared mediators including p21, p53 and p16INK4a, the RT-activated senescence program in tumor cells would also substantially enhance their stemness features in a cell-autonomous manner, leading to significant enhancement in the self-renewal and invasive capability to facilitate post-treatment relapse 105. The gene discussed is CDKN2A; the disease is neoplasm.