Regardless of direct cellular cross‐talk, the continuous release of different agonists, including thrombin and ADP, by both tumor cells and developing thrombi, as well as tumor‐released cytokines, including TNF‐α and IL‐1β, enhance platelet activation and adhesion while impairing the antithrombotic responses of endothelial cells. This evidence concerns the gene IL1B and neoplasm.