A team from Würzburg has fundamentally changed our understanding of platelet biology with a study published in Science. The researchers demonstrate that the surface protein integrin αIIbβ3 is not only a key molecule in blood clotting, but can also act as a pro-inflammatory effector during severe disease processes. Under these conditions, αIIbβ3 switches function and becomes a structural component of a previously unknown organelle: PITT (Platelet-derived Integrin- and Tetraspanin-rich Tether). PITTs are released by platelets, remain deposited at the inflamed vessel wall, and further drive inflammatory processes. Blocking αIIbβ3 with monoclonal antibodies reduces PITT formation.