In contrast to the inhibition of osteoblastic bone formation in myeloma and breast cancer mouse models by activin A [96, 97], it has been demonstrated very recently that, in fibrodysplasia ossificans progressive (FOP), a constitutively activating mutation (R206H) of the bone morphogenetic protein type 1 receptor activin-like kinase 2 (ACVR1/ALK2) leads to an extensive ossification of skeletal muscle, fascia, ligaments and tendons. The gene discussed is ACVR1; the disease is fibrodysplasia ossificans progressiva.