In the same study, the authors described the suppression of HO formation by treatment with these molecules in vivo, in mice implanted with FOP-iPSCs cells together with a source of ActA [37], thus providing the basis for a possible repurposing of mTOR inhibitors in the management of FOP (see also section “Targeting the microenvironment of FOP local lesions” for results described by Kaplan et al. [38]). Here, ACTA1 is linked to fibrodysplasia ossificans progressiva.