Notably, elevated expression of IL-17, the signature cytokine of Th17 cells, temporally mirrored ILC3 expansion after TBI (38), while loss of T-bet in NKp46+ ILCs impaired the CNS infiltration of myelin-reactive Th17 cells, reduced neuroinflammation, and attenuated white matter loss within the spinal cord using a murine model of multiple sclerosis (39). The gene discussed is IL17A; the disease is multiple sclerosis.