After the discovery of ACVR1/Alk2 as the causative gene in FOP, this mouse was considered useful to model the disease phenotype, since intramuscular expression of the caAlk2 transgene was able to induce ectopic endochondral bone formation with joint fusion and functional impairment [55]. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.