Platelets, which are vital for blood clotting and immunity, need to maintain a delicately balanced relationship between generation and destruction. Recent studies have highlighted that reactive oxygen species (ROS), which act as second messengers in crucial signaling pathways, are crucial players in this dance. This review explores the intricate connection between ROS and platelets, highlighting their dual nature. Moderate ROS levels act as potent activators, promoting megakaryocyte (MK) differentiation, platelet production, and function. They enhance platelet binding to collagen, increase coagulation, and directly trigger cascades for thrombus formation. However, this intricate role harbors a double-edged sword. Excessive ROS unleash its destructive potential, triggering apoptosis and reducing the lifespan of platelets. High levels can damage stem cells and disrupt vital redox-dependent signaling, whereas uncontrolled activation promotes inappropriate clotting, leading to thrombosis. Maintaining a precise balance of ROS within the hematopoietic microenvironment is paramount for optimal platelet homeostasis. While significant progress has been made, unanswered questions remain concerning specific ROS signaling pathways and their impact on platelet disorders. Addressing these questions holds the key to unlocking the full potential of ROS-based therapies for treating platelet-related diseases such as thrombocytopenia and thrombosis. This review aims to contribute to this ongoing dialog and inspire further exploration of this exciting field, paving the way for novel therapeutic strategies that harness the benefits of ROS while mitigating their dangers.