The underlying mechanism of ActivinA/SMAD1/5 signaling is not fully understood but suggests ACVR1 dependency and independency of ACVR1B/C/TGFBR1 as demonstrated by inhibitor experiments in FOP iECs being in line with knockdown studies in FOP [12] and myeloma cells [47]. This evidence concerns the gene ACVR1B and plasma cell myeloma.