We focused on two genetic disorders, ataxia telangiectasia (AT), a severe neurodegenerative syndrome caused by gene defects in ATM (ataxia telangiectasia mutated) which is essential for DSB repair, and Hutchinson–Gilford progeria (HGPS or PS), which exhibits premature aging symptoms due to a mutation in LAMIN A (LMNA) that maintains nuclear architecture. This evidence concerns the gene LMNA and hereditary disease.