Induction of IRF-1 protein by either ionizing radiation or etoposide occurs through an increase in IRF-1 protein levels and an increase in the half-life of the IRF-1 protein; the response requires a functional DDR as cells defective in the DNA damage sensor ATM (ataxia telangiectasia, mutated) failed to increase IRF-1 in response to genotoxic stress (Pamment et al., 2002). This evidence concerns the gene IRF1 and Telangiectasia.