Most human progeroid syndromes result from monogenic defects in nuclear components (Kubben and Misteli, 2017) (e.g. LMNA in Hutchinson-Gilford progeria syndrome, TERC in dyskeratosis congenita), and telomere length has long been observed as a marker of aging (Garcia et al., 2007). The gene discussed is LMNA; the disease is Hutchinson-Gilford progeria syndrome.