In our cases, ORFV-lesioned tissues significantly overexpressed IL-6, which is a multifunctional cytokine implicated in many proinflammatory functions, but also in promoting cell survival, apoptosis, and proliferation, with the level of IL-6 significantly increased in several tumors.11,14,17 Accordingly, EGFR activates transcription of IL-6 in liver macrophages contributing to hepatocellular carcinoma development.18 These findings suggest that this cytokine is involved in the molecular mechanism leading to the atypical proliferative changes seen in some ORFV infections. The gene discussed is IL6; the disease is hepatocellular carcinoma.