TTM, previously known as an anti-cancer Cu chelator when used as a single agent [46] paradoxically also helped revert apoptosis-associated PARP cleavage mediated by DSF and SOD, implying that basal Cu sequestration by TTM from DSF diminishes the latter ROS-inducing ability (47), implying that Cu bound to TTM behaves very differently to Cu bound to DSF. The gene discussed is SOD1; the disease is cancer.