ACVR1 and fibrodysplasia ossificans progressiva: However, it is unclear if human FOP ECs can transdifferentiate into osteogenic cells and directly contribute to bone formation, if another mechanism leads to the increase in ECs in FOP lesions [7, 9], if ECs are crucial in the very early steps of heterotopic ossification, or if human FOP ECs also respond abnormally to BMP or Activin A signals acting on the ACVR1 R206H receptor [11, 12].