Your critical commentary about our recent paper in the Laser in Surgery and Medicine (2000;27:420ยฑ426) is valuable to understand the induction of damage by lowdensity laser irradiation in the mouse model. The clear initiating event of oxidative stress should be noted for its relationship to thrombus formation because the production of oxygen-free radicals generated from the oxidative stress is a major cause of endothelial injury and of the alterations in clotting [1,2] including platelet recruitment [3]. It means that such antioxidants as superoxide dismutase (SOD) and catalase may reduce the thrombus growth and their functional roles may be adjusted by low intensity laser irradiation on dose-dependent manner. Therefore, if laser irradiation generates the superoxide, thrombosis can possibly occurred. We assumed the thrombus growth may be a reยฏection of platelet recruitment by oxygen radicals generated. Previous experimental thrombosis model induced by free radicals clearly supports the fact that free radicals always induce thrombosis and the induced thrombus was mainly composed of platelets under ยฎltered light [4]. In conclusion, although low doses of laser were found to stimulate the regeneration of induced wound, we could not doubt that thrombosis occurred by laser irradiation. Therefore, it should be emphasized for further clinical implication.