These anti-inflammatory properties of IKK/NF-κB signalling could explain the initially unexpected increase in atherosclerosis in hyperlipidaemic Ldl receptor (Ldlr)-deficient mice with a myeloid-specific deletion of Ikkβ, which was linked to a significant reduction of the anti-inflammatory cytokine IL-10 in Ikkβ−/− macrophages [11]. The gene discussed is IKBKB; the disease is atherosclerosis.