After global postnatal induction of mutated ACVR1 in ACVR1R206H/+ transgenic [87] and knock-in mice [88, 89], HO is formed in the skeletal muscle of activin A administration sites [87, 88], or cardiotoxin injury sites [89], or even spontaneously in mirroring sites that commonly ossify in FOP patients [88, 89]. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.