Numerous clinical studies have highlighted the pro‐tumorigenic effects of IL‐1α and IL‐1β, in which IL‐1β stimulates inflammatory mediators, promotes cellular invasion and immunosuppression.[32, 33] Additionally, TNF exhibits diverse tumor‐promoting activities, such as stimulating cytokine cascade responses, fibrotic responses, and altering adhesion receptors.[34] These findings imply that BBR treatment could alter the transcriptional profiling of immune cells and prevent HCC progression through influencing the secretion of cytokines. This evidence concerns the gene IL1A and neoplasm.