A role in this scenario could be also played by BM MSCs which exert immune suppressive activities in the MM microenvironment, being involved in ADO release through CD31/CD73/CD203a pathway expressed on their surface and also by promoting MM cell proliferation and T cell inactivation via PD-L1/PD-1 axis [34]. The gene discussed is PDCD1; the disease is Miyoshi myopathy.