An electrophysiological hallmark of Parkinson’s disease (PD) is abnormal oscillatory activity, most notably excessive synchronization in the beta band (12-20 Hz). These oscillations are seen throughout the cortical-subcortical motor circuitry, and historically have been thought to arise within the basal ganglia (BG). However, recent theoretical and experimental studies have suggested a cortical origin for the abnormal activity. As such, a substantial scientific effort is currently focused on characterizing cortical activity in the parkinsonian state, as well as its modulation by deep brain stimulation (DBS). Hyperdirect neurons have been identified as key players in this puzzle because of their unique anatomical connections and powerful influence over network activity. Hyperdirect neurons are a special subset (~5%) of layer V pyramidal neurons whose corticofugal axon projects down internal capsule and into the spinal cord, while also sending an axon collateral to the subthalamic nucleus (STN). One prevailing hypothesis is that pathological beta activity arises within cortex and is transmitted into the BG via the hyperdirect pathway. In line with this hypothesis, selective optogenetic stimulation of the hyperdirect pathway is sufficient to alleviate parkinsonian symptoms in rodents and numerous recent clinical DBS studies have come to a similar conclusion in humans. My presentation will provide an overview of experimental work analyzing the hyperdirect pathway, followed by new modeling results on DBS of this pathway and its subsequent effect on cortical network activity.