It has been postulated that Tregs are implicated in MM progression on the basis of their contribution to the complex immunosuppressive environment through the secretion of IL-10 and TGF-β by APRIL/TACI-dependent mechanisms and through the CD39/CD73 adenosine pathway and direct inhibition of effector T cell responses [59]. Here, TGFB1 is linked to Miyoshi myopathy.