Though phospholipase C PLCγ2 is known to play an important role in platelet activation by collagen and fibrinogen, its importance in GPIb‐mediated platelet activation is less well understood. To better understand the role of PLCγ2 in GPIb‐mediated adhesion and thrombus formation, we examined the ability of wild‐type and PLCγ2‐ deficient murine platelets to spread on immobilized von Willebrand factor (VWF) under static conditions, and to attach to and form thrombi on VWF under conditions of arterial shear. While absence of PLCγ2 had only a minimal effect on platelet adhesion to immobilized VWF, its absence impaired spreading and profoundly affected thrombus growth and stability on VWF.