Recently, it has been proven that platelets can migrate independently against the bloodstream. Similar to platelet spreading, talin binding shifts integrin αIIbβ3 into an activate mode that can interact with ligands. Integrin αIIbβ3 ligand binding-mediated outside-in signaling initiates branching of the actin mesh at the platelet rim and the protrusion of the platelet edge. Myosin-mediated contraction of stress fibers within the cell body leads to forward movement of the trailing edge. Platelets migrate along the integrin αIIbβ3 ligand gradient toward higher ligand concentrations, by applying a haptotaxis mode of migration. During the retraction of the platelet body, integrin αIIbβ3 ligand can be scavenged, thereby creating a ligand gradient underneath the platelet and a positive feedback loop for migration. Platelet migration can be induced by agonists, such as ADP or TxA2, or a chemotactic stimulus, but these stimuli are not necessary to initiate or uphold platelet migration. Migrating or polarized platelets with lamellipodia have been observed in inflamed vessels and tissues but not within thrombi. These migrating platelets have been demonstrated to safeguard the microvasculature by scanning and sealing microlesions as well as removing active phase proteins such as fibrinogen. Furthermore, they collect and bundle bacteria to facilitate PMN phagocytosis and NET formation. Hence, mammalian platelets have been demonstrated to have a dual function in hemostasis and the innate immune response.