On the one hand, the deletion of exon 27 would disrupt the 17th cb-EGF domain of FBN2, affect the binding of the cb-EGF domain to calcium ions, and make fibrillin-2 more susceptible to hydrolysis; on the other hand, disruption of the 17th cb-EGF domain may alter the spatial conformation and intermolecular interactions of proteins (Xu et al. 2019), and eventually lead to CCA. This evidence concerns the gene EGF and congenital contractural arachnodactyly.