Lesions in the caudal fastigial nucleus (cFN) severely impair the accuracy of visually guided saccades in the head-restrained monkey. Is the saccade dysmetria a central perturbation in issuing commands for orienting gaze (eye in space) or is it a more peripheral impairment in generating oculomotor commands? This question was investigated in two head-unrestrained monkeys by analyzing the effect of inactivating one cFN on horizontal gaze shifts generated from a straight ahead fixation light-emitting diode (LED) toward a 40 degrees eccentric target LED. After muscimol injections, when viewing the fixation LED, the starting position of the head was changed (ipsilesional and upward deviations). Ipsilesional gaze shifts were associated with a 24% increase in the eye saccade amplitude and a 58% reduction in the amplitude of the head contribution. Contralesional gaze shifts were associated with a decrease in the amplitude of both eye and head components (40 and 37% reduction, respectively). No correlation between the changes in the eye amplitude and in head contribution was observed. The amplitude of the complete head movement was decreased for ipsilesional movements (57% reduction) and unaffected for contralesional movements. For both ipsilesional and contralesional gaze shifts, the changes in eye saccade amplitude were strongly correlated with the changes in gaze amplitude and largely accounted for the gaze dysmetria. These results indicate a major role of cFN in the generation of appropriate saccadic oculomotor commands during head-unrestrained gaze shifts.