Lesions of the posterior parietal cortex in humans can produce a specific disruption of visually guided hand movements termed optic ataxia. The fact that the deficit mainly occurs in peripheral vision suggests that reaching in foveal and extrafoveal vision relies on two different anatomical substrates. Using fMRI in healthy subjects, the authors demonstrated the existence of two systems, differently modulated by the two reaching conditions. Reaching in central vision involves a restricted network, including the medial intraparietal sulcus (mIPS) and the caudal part of the dorsal premotor cortex (PMd). Reaching in peripheral vision engages a more extensive network, including the parieto-occipital junction (POJ). Interestingly, POJ corresponds to the site of the lesion overlap that the authors recently found to be responsible for optic ataxia. These two sets of results converge to show that there is not a unique cortical network for reaching control but instead two systems engaged in reaching to targets in the central and peripheral visual field.