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Cells from these patients display increased oxidative stress as a consequence of elevated levels of ROS, increased oxidized/reduced glutathione (GSSG/GSH) ratio, diminished capacity to scavenge ROS and mitochondrial dysfunction.1812 Furthermore, ATM is directly activated by oxidative stress19 and can exert antioxidant activity through regulation of the pentose-phosphate pathway.20 Recent evidence suggests that ATM might regulate oxidative stress through NRF2

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As expected the reduced platelet count was accompanied by decreases in ATP, ADP and thromboxane A 2 levels, factors derived from platelets, while plasma thrombin level was not changed significantly (Supplementary Fig

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