It is possible that the high circulating sTNFRII levels observed in our patient cohort reflect “hyper-activation” of the TNF system secondary to chronic hepatitis and HCC, contributing to a potent pro-inflammatory systemic milieu and resulting in more severe liver injury and subsequent liver toxicity plus increased risk of death at 3 months after completion of SBRT. The gene discussed is TNF; the disease is hepatocellular carcinoma.