HMGB1 and Miyoshi myopathy: Therapeutic levels of ASA and SA suppressed the migration, invasion, wound healing, EMT signaling and anchorage-independent colony formation of HMGB1-secreting MM cells but not those of MM cells, which secrete low to undetectable amounts of HMGB1, suggesting that the antitumor activity of ASA/SA was related to HMGB1 (Figures 2, 3, 4).