It is tempting to speculate that this ATM function is particularly critical for post-mitotic tissues and may account, in part, for the progressive neurological phenotype of Ataxia Telangiectasia (AT) patients, in which mutant or absent ATM cannot trigger a proper cellular response to the gradual accumulation of metabolically derived (or endogenously produced) DNA lesions.42,43. This evidence concerns the gene ATM and Ataxia-telangiectasia.