The recent discovery that activin A induces p‐Smad1 signaling via mutant ALK2, has expanded the potential therapeutic strategies to prevent HO signaling in FOP (reviewed in37), including impairment of the activin A‐ALK2 complex formation by means of ligand traps of neutralizing antibodies, genetic downregulation of ACVR1, and mutant ALK2 kinase‐activity inhibition. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.