In the last decade, transforming growth factor-beta 1 (TGF-β1) has been recognized as a key driver in liver fibrosis, resulting in a higher risk of HCC development.4–5,6 TGF-β1 has a double-sword role in many cancers including HCC: as an onco-suppressor it inhibits cell proliferation, whereas as a tumor promoter it triggers the epithelial–mesenchymal transition, which facilitates tumor spread and metastasis because of a downregulation of E-cadherin.7, 8 The mechanisms regulating the switch from onco-suppressor to tumor promoter are still debated. This evidence concerns the gene TGFB1 and neoplasm.