Based on these insights, we posited that while intratumoral inflammatory mediators (e.g., IL-6, TNF-α, and IL-1β) could modulate antitumor immunity and angiogenesis, thus influencing tumor progression and MVI onset [32], the overall patient systemic status often confounds systemic inflammatory indices in peripheral blood, limiting the clinical utility for predicting the MVI/Ki-67 status in HCC. The gene discussed is IL1B; the disease is neoplasm.