Accordingly, we sought to determine whether inhibition of NQO1-induced c-Fos/CKS1 expression leads to increased radiosensitivity through accumulation of cancer cells at the G2/M phase by assessing clonogenic survival; quantifying γH2AX foci, a marker of DNA double-strand breaks (DSBs) and activation of the DNA damage response; and performing homologous recombination (HR) and non-homologous end joining (NHEJ) assays. The gene discussed is FOS; the disease is cancer.