Specifically, it is unclear whether the mutant ACVR1 in macrophages can directly activate and modulate downstream inflammatory signaling pathways via Activin A. Furthermore, it is necessary to investigate whether Activin A, as a key mediator of fibrosis, extends the functional role of fibroblasts in the pathogenesis of FOP. This evidence concerns the gene ACVR1 and fibrodysplasia ossificans progressiva.