These unpublished results from HF‐stretch experiments opened a prologue toward verification of a possible inhibitory mechanism that is centered on a post‐translational modification of released HGF and/or ECM‐bound HGF and differs from high‐HGF concentration‐induced expression of myostatin that re‐establishes satellite cell quiescence (Yamada et al., 2010). The gene discussed is MSTN; the disease is hydrops fetalis.