A study from the University of Cambridge and international collaborators explains the potential molecular mechanism behind aspirin's antineoplastic effects. Researchers identified an immunosuppressive pathway involving platelet-derived thromboxane A2 activation of the TP receptor on T cells, leading to immune surveillance suppression against cancer metastasis. The findings provide mechanistic insights into the anti-metastatic activity of aspirin and suggest potential strategies for enhanced anti-metastatic therapy.