Our data showed that the over-expression of either kinase-deficient ActR-IIAK219R or ActR-IIBK217R as well as their combination significantly downregulated activin A-induced BMP signaling via ALK2R206H, suggesting that the kinase activity of the type II receptor is required for activin A-induced BMP signaling in FOP disease (Figure 6A). The gene discussed is NCOA3; the disease is fibrodysplasia ossificans progressiva.