This may imply that ATF3 induces cell cycle arrest by affecting NF-κB-related pathways either directly through binding to the p65 subunit of NF-κB and thus inducing its subsequent attenuation or indirectly by eliciting the regulation of matrix metalloproteinase (MMP) expression and the inhibition of the nuclear translocation of NF-κB in glioblastoma cells as Guenzle et al. reported earlier [36]. The gene discussed is NFKB1; the disease is glioblastoma.