Results in this work show that STAT pathway genes are upregulated in cycling MSCs after muscle or tendon injury, especially targets of Stat3 and Stat1 known to play a role in cell proliferation among other processes.[51] Interestingly, inhibition of JAK1/2 could prevent neurogenic HO.[52] We noted that both traumatic HO and FOP share some common features in pathology, i.e., injury‐induced inflammatory response will promote or accelerate heterotopic endochondral bone formation in the soft tissues. The gene discussed is SOAT1; the disease is fibrodysplasia ossificans progressiva.