The study also showed that Ectonucleotide Pyrophosphatase/Phosphodiesterase 2 (ENPP2), a known mTOR signaling activator, mediated mTORC1 signaling activation by Activin A. Furthermore, mTOR inhibition by rapamycin potently blocked the enhancement of chondrogenesis in vitro and HO formation in the FOP mouse model triggered by Activin A. Rapamycin has been shown to inhibit HO in separate mouse models, including both trauma-induced and genetic HO in FOP [58]. The gene discussed is ENPP2; the disease is fibrodysplasia ossificans progressiva.