Several potential sources of ROS have been suggested, including NADPH oxidase and the mitochondrial respiratory chain [15]. NADPH oxidase-derived ROS play an important role in agonist-stimulated platelet activation [32,33]. Moreover, several reports support a role for NADPH oxidase in hyperthermia-induced tumor cell apoptosis [19,20]. In order to investigate the sources of ROS in hyperthermia-treated platelets, we first studied the effect of NADPH oxidase in hyperthermia-induced ROS production. We used the NADPH oxidase inhibitors DPI and apocynin. We found that DPI partially inhibited ROS generation in hyperthermia-treated platelets, whereas apocynin did not (Figure 1C), suggesting that NADPH oxidase might play an insignificant role in hyperthermia-induced ROS production.