Furthermore, also in line with our original hypothesis, HO in FOP involves a ligand that not only activates ACVR1[R206H] (and all the other FOP-causing variants of ACVR1) but it is also regulated by inflammation, and recognized by tissue-resident progenitor cells that can give rise to heterotopic bone via an endochondral process. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.