During EndMT, endothelial‐specific markers, such as tyrosine kinase with immunoglobulin‐like and EGF‐like 1 (Tie‐1), vascular endothelial cadherin (VE‐cadherin) and CD31 are reduced, but mesenchymal‐specific markers, such as fibroblast‐specific protein 1 (FSP‐1), neural cadherin (N‐cadherin) and α smooth muscle actin (α‐SMA), increase.10 Previous studies indicated that endothelial cells from FOP lesions undergo inflammation‐induced EndMT, acquire a mesenchymal stem‐like phenotype and subsequently differentiate into osteoblasts suggesting the critical role of EndMT in HO formation. This evidence concerns the gene CDH2 and fibrodysplasia ossificans progressiva.