Our previous preclinical studies demonstrated that BTZ treatmentinduces MM cell aggressiveness via host cell activity rather thanvia direct effects on cancer cells8,9 Specifically,plasma from BTZ-treated mice induced MM cell migration and proliferation in vitro.(8) Furthermore, we foundthat BTZ treatment elevates the levels of M1 pro-inflammatory macrophagesin the bone marrow where they secrete factors that support MM cellaggressiveness.8,9 Given these findings, we soughtto determine whether ATBL induces pro-tumorigenic activities, similarto free BTZ. Here, CASC3 is linked to Miyoshi myopathy.