However, it must also be noted that while the targeting IKK2 holds promise as a likely anti-inflammatory therapy, it was found that pharmacological IKK2 inhibition can also result in increased endotoxin susceptibility that is associated with increased levels of IL-1β as a result of increased pro-IL-1β secretion by macrophages and neutrophils upon bacterial infections, thereby causing overt systemic inflammation and lethality in mice [143]. This evidence concerns the gene IL1B and bacterial infectious disease.