Of note, numerous recent studies have reported phosphorylation of RIPK1 mediated by TAK1, MAP kinase-activated protein kinase 2 (MK2), TBK1 (TANK binding kinase 1)/IKKε and IKKα/β provide a physiological brake to prevent TNF-induced RIPK1 kinase-dependent cell death during embryogenesis, infection, and neuroinflammation19–26. The gene discussed is MAPKAPK2; the disease is infection.