when an ischemic event occurs, IκB is phosphorylated and degraded, which induces the activation of NF-κB contributing to transcription of many pro-inflammatory genes that encode cytokines, chemokines, and enzymes such as TNF-α, IL-6, IL-1β and iNOS, these mediators are implicated in the progression of neonatal cerebral inflammation after HI injury [43]. This evidence concerns the gene IL1B and inflammatory response.