Specifically, radiation, rather than HFD, aggravated HFD-induced atherosclerosis by activating the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signalling pathway through phosphorylation of TANK-binding kinase 1 (TBK1) and interferon regulatory factor 3 (IRF-3), leading to increased expression of pro-inflammatory mediators IL-1β, IL-18, IFNα, and IFNβ, thereby promoting atherosclerotic plaque formation [100]. The gene discussed is IL1B; the disease is atherosclerosis.