Our results are of great interest for orthopedic research, as alterations in FN1 or in the FN1-triggered activation of integrins, both of which we assume to depend on extracellular ERp57 activity, are associated with skeletal diseases such as OA or spondylometaphyseal dysplasia (SMD) with corner fractures.16 The gene discussed is FN1; the disease is spondyloepimetaphyseal dysplasia, Strudwick type.