Given that Fgr was coexpressed with p65, ERK1/2, and TNF-α, and that p65 was also coexpressed with TNF-α in thalamic microglia under hemorrhagic stroke conditions, Fgr likely participates in the hemorrhage-induced microglial activation and subsequent production of TNF-α via the activation of both NF-κB and ERK1/2 pathways. The gene discussed is NFKB1; the disease is hemorrhagic stroke.