ZMPSTE24 and alopecia: In 2002, two laboratories developed the Zmpste24−/− mouse model, which lacks the metalloprotease ZMPSTE24 responsible for cleaving the farnesylated and carboxymethylated C-terminus of prelamin A. Homozygous Zmpste24−/− mice accumulate irreversibly modified prelamin A, lack mature lamin A, and develop a bona fide progeroid phenotype, including muscle and bone defects, alopecia, lipodystrophy, cardiac alterations, and reduced lifespan [35,38,39].