Traumatic brain injury (TBI) is a significant worldwide cause of morbidity and mortality. A chronic neurologic disease bearing the moniker of "the silent epidemic," TBI currently has no targeted therapies to ameliorate cellular loss or enhance functional recovery. Compared with those of astrocytes, microglia, and peripheral immune cells, the functions and mechanisms of NG2-glia following TBI are far less understood, despite NG2-glia comprising the largest population of regenerative cells in the mature cortex. Here, we synthesize the results from multiple rodent models of TBI, with a focus on cortical NG2-glia proliferation and lineage potential, and propose future avenues for glia researchers to address this unique cell type in TBI. As the molecular mechanisms that regulate NG2-glia regenerative potential are uncovered, we posit that future therapeutic strategies may exploit cortical NG2-glia to augment local cellular recovery following TBI.