Several observations are consistent with NF-κB activation during neonatal sepsis [15, 16], and in a mouse model of group B Streptococcus neonatal sepsis, the pathway mediated by c-Jun N-terminal kinase was demonstrated to play a pivotal role in the orchestration of inflammation during sepsis, as its inhibition significantly suppressed proinflammatory cytokines production [17]. This evidence concerns the gene NFKB1 and Neonatal sepsis.