ATM and ataxia telangiectasia: Similarly, dysfunction of ataxia-telangiectasia mutated (ATM), a serine/threonine kinase critically involved in the response to and repair of DNA double-strand breaks, provokes the accumulation of damaged DNA in the cytosol, which results in constitutive STING-dependent type I IFN production, contributing to the inflammatory phenotype characteristic for the cancer-prone disease ataxia-telangiectasia (17).