This hypothesis is based on the startling absence of degenerative symptoms in mice deficient in expression of genes linked to hereditary degenerative diseases in humans, such as (i) ataxia-telangiectasia, which is characterized by ATM mutational inactivation; (ii) Bloom syndrome, resulting from a mutation in the RecQ helicase family member BLM; and (iii) Duchenne muscular dystrophy (DMD), resulting from dystrophin, DMD mutation. Here, ATM is linked to Duchenne muscular dystrophy.