All in all, targeting the JAK/STAT metabolic pathway in HCC may be a useful therapeutic option, as it involves several oncogenic and progression-promoting mechanisms typical of HCC, such as chronic inflammation (Fibrosis is associated with oncogenesis and the development of HCC [324,325]), altered metabolism (STAT3 activation enhances the Warburg effect by promoting anaerobic glucose metabolism [326]), and angiogenesis [297,327,328]. This evidence concerns the gene STAT3 and hepatocellular carcinoma.