Specifically, HO in FOP are caused by gain-of-function dominant missense mutation of the ACVR1 gene encoding a type 1 bone morphogenetic protein receptor,48–50 whereas NHO are in part driven by excessive adrenergic signaling as a consequence of a SCI.51 Which molecular events are permissive to HO development after severe burn injuries remain yet to be determined. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.