In patients with either Marfan syndrome or acromicric dysplasia there is reportedly an increase in bioactive TGFβ due to its decreased binding by fibrillin 1, which is responsible in part for the clinically disparate manifestations of these disorders, although the mechanism(s) that underlie the opposite clinical manifestations of these disorders remains unknown at present (10). Here, FBN1 is linked to Acromicric dysplasia.