Contrarily, Roger et al. showed that the proinflammatory macrophage migration inhibitory factor MIF contributed to detrimental hyperinflammation during sepsis.35 Similarly, Heinemann et al. found a specific population of inflammatory monocytes in neonates that are regulated/ suppressed by S100A8/A9 alarmins.36 Together with our present results, it can be assumed that neonatal monocytes do not have an intrinsically decreased inflammatory capacity but that this is rather controlled by extrinsic factors. The gene discussed is IGKV1D-22; the disease is Sepsis.