The caudal fastigial nucleus (CFN) is critical for generating accurate saccades toward a visual target. Its pharmacological inactivation alters the amplitude of their horizontal component: it is hypermetric for ipsilesional saccades and hypometric for contralesional ones. A recent study reported that "ipsilesional saccades showed more endpoint variability than did normal saccades" and that the "inactivation effects on saccade noise are explained by a decrease of the feedback gain and an increase of planning and/or signal dependent motor noise" (Eggert et al., 2016). In the framework of a control of saccade amplitude by negative feedback, the hypermetria of the horizontal component of ipsilesional saccades can indeed be explained by an underestimation of the current eye displacement. However, instead of adding a notion which is rather neurophysiologically undetermined (“noise”), we propose that the endpoint variability actually reflects the size of the active population in the CFN. This conjecture derives from the results from Quinet & Goffart (2015) who showed that the size of saccades evoked by electrical microstimulation in the fastigial nucleus increases with larger current. According to this hypothesis, if an injection of muscimol is made not exactly centered in the fastigial oculomotor region, the number of saccade-related neurons which are inactivated by the pharmacological agent should increase as it diffuses, resulting in a time-varying dysmetria. Moreover, this effect of diffusion should not be restricted to the generation of ipsilesional saccades, but should concern also the generation of contralesional ones. We will show examples of inactivation experiments performed in head-restrained monkeys where the magnitude of dysmetria did not change with time and others where it increased. Depending upon the experiment, this time-varying effect affected either ipsilesional or contralesional saccades. Thus, the so-called “noise” inferred from the variability of endpoints after CFN inactivation seems to result from an increase of the number of neurons which are silenced by the pharmacological agent (muscimol). The possibility to independently alter the horizontal component of ipsilesional or contralesional saccades suggests independent output channels from the CFN to the saccade-related premotor neurons. More fundamentally, these observations point to the fact that the size of the population of active neurons in the CFN plays a major role in the cerebellar control of the horizontal amplitude of saccades: it participates to their dynamics by recruiting the appropriate number of premotor burst neurons, excitatory and inhibitory.