Two non-mutually exclusive possibilities may explain the increased interhemispheric inhibition following stroke: (i) a structural reorganization of callosal fibres, with enhanced innervation of NGF cells and, possibly, a retraction of inputs onto the dendrites of local pyramidal cells; (ii) an enhanced synaptic transmission between transcallosally-driven interneurons and cortical pyramids. The gene discussed is NGF; the disease is stroke disorder.