Indeed, this force‐dependent mechanism is supported by experiments that demonstrated both external stretching or increasing intracellular tension directly activate latent TGF‐β1 from the latent TGF‐β binding protein‐1 (LTBP‐1) in the extra cellular matrix.[26, 38] Although involvement of TGF‐β signaling in pathogenesis of tendinopathy has been reported, we are the first to demonstrate that integrin αvβ6 activation of excessive TGF‐β1 is the molecular mechanism of tendinopathy. The gene discussed is TGFB1; the disease is disease of the tendon.