Similarly, transgenic mice overexpressing ACVR1Q207D, another activating mutation, only developed heterotopic ossification in the presence of the type II receptors ACVR2A and BMPR2, demonstrating a requirement of the type II receptors for the pathology of mutant ACVR1 in FOP (Bagarova et al,2013). Here, ACVR1 is linked to fibrodysplasia ossificans progressiva.