H2AX and Miyoshi myopathy: Notably, despite a significant reduction in ROS levels, the antioxidant did not protect MM cells from trabectedin-induced apoptosis and DNA damage, evaluated as H2AX protein phosphorylation (γ-H2AX) (Fig. 3d), demonstrating both effects (DNA damage and apoptosis) to be independent from ROS production (representative dot plots of U266 and MM1S MM cells reporting trabectedin activity in term of apoptosis in presence or absence of trabectedin and/or ascorbic acid, were showed in Additional file 5: Figure S4B).