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 This evidence concerns the gene PDIA3 and bone disorder.