It has been previously proposed [3] that mutations in genes affecting the interaction with the EGF domain (which are highly expressed during lens development) are the mechanism behind lenticular abnormalities in Traboulsi syndrome, as virtually all genes implicated in lens subluxation (FBN1, ADAMTSL4, ADAMTS10, and ADAMTS17) encode proteins that interact with EGF [3]. This evidence concerns the gene EGF and facial dysmorphism-lens dislocation-anterior segment abnormalities-spontaneous filtering blebs syndrome.