MAD can be classified into type A and B: mutations in lamin A that affect processing by ZMPSTE24 belong to type A, whilst mutations that impair the proteolytic activity of ZMPSTE24 are classified as type B. Both types share clinical features that resemble progeria but vary in severity; whilst patients with progeria display signs of aging 1–2 years after birth, patients with MAD generally develop abnormalities around the age of ∼4–5 years. Here, ZMPSTE24 is linked to mandibuloacral dysplasia.