HIF1A and fibrodysplasia ossificans progressiva: We further showed that early inflammatory FOP lesions in humans and in a mouse model are markedly hypoxic, and the inhibition of HIF-1α by genetic or pharmacologic means restores canonical BMP signaling to normoxic levels in human FOP cells and profoundly reduces HO in a constitutively active CA-AVCR1 (Q207D) mouse model of FOP.