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61 Marta Muzio’s team identified IRAK-2 and MYD88 innate immune signal transduction adapter (MyD88) as mediators for IL-1R-induced NF-κB signaling, and MyD88 serves as a signal transduction adapter to mediate the binding of IRAK to IL-1R, which provides possible targets for the treatment of inflammatory diseases

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193 Finally, genetic epidemiology strengthens causal inference: Mendelian randomization analyses of circulating inflammatory mediators identify specific inflammatory axes that appear causally linked to cancer risk (e.g., pro-adrenomedullin for BC), indicating that inflammation is not merely an epiphenomenon of adiposity but part of the causal pathway for certain cancers