In 2006, a heterozygous gain of function mutation (c.617G>A; R206H) in the glycine-serine (GS) domain of the activin A receptor type I (ACVR1), also known as activin receptor-like kinase 2 (ALK2), was identified as the genetic cause of FOP [13]. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.