The contribution of the posterior parietal cortex (PPC) to visually guided movements has been originally inferred from observations made in patients suffering from optic ataxia. Subsequent electrophysiological studies in monkeys and functional imaging data in humans have corroborated the key role played by the PPC in sensorimotor transformations underlying goal-directed movements, although the exact contribution of this structure remains debated. Here, we used transcranial magnetic stimulation (TMS) to interfere transiently with the function of the left or right medial part of the intraparietal sulcus (mIPS) in healthy volunteers performing visually guided movements with the right hand. We found that a "virtual lesion" of either mIPS increased the scattering in initial movement direction (DIR), leading to longer trajectory and prolonged movement time, but only when TMS was delivered 100-160 ms before movement onset and for movements directed toward contralateral targets. Control experiments showed that deficits in DIR consequent to mIPS virtual lesions resulted from an inappropriate implementation of the motor command underlying the forthcoming movement and not from an inaccurate computation of the target localization. The present study indicates that mIPS plays a causal role in implementing specifically the direction vector of visually guided movements toward objects situated in the contralateral hemifield.