Moreover, Tmem119-CreERT2; Nr4a1fl/fl mice phenocopied Nr4a1-/- mice and showed a larger infarct size and worse neurological deficits than those in Nr4a1fl/fl littermates after stroke, while Etanercept (ETA, a dimeric Fc-fusion protein that specifically target TNF-α) treatment significantly reduced the infarct size and attenuated neurological deficits in Tmem119-CreERT2; Nr4a1fl/fl mice, suggesting that increased TNF-α was the major contributing factor that mediate pro-damaging effect of Nr4a1-knockout in microglia (Fig 6E–6I). The gene discussed is TMEM119; the disease is stroke disorder.