Since mice appear to be more resistant to progerin accumulation than humans, the homozygous LmnaG609G/G609G mouse model has been employed because it develops a severe progeroid phenotype earlier than heterozygous LmnaG609G/+ mice, thereby more closely reflecting the situation in the progeria patients presenting with heterozygous mutations [32, 75]. The gene discussed is LMNA; the disease is progeroid syndrome.