Results from our bioinformatic analysis suggest that ΔFosB via its downstream targets like Cxcl12 (Stephens et al., 2020), a chemokine with confirmed role in epilepsy (Song et al., 2016; Zhou et al., 2017; Xu et al., 2019) could suppress further worsening of neuroinflammation in epileptic brain but we cannot rule out a possibility that increased gliosis is a consequence of mossy fiber degeneration or granule cell dispersion or combination of these processes. This evidence concerns the gene CXCL12 and epilepsy.