This model highlighted the potential of cancer cells to change gene expression in response to immune interaction and detailed a comprehensive analysis of the mechanism underlying HCC progression via the activation of the JAK/STAT pathway in tumour cells by the human immune system, implying that the DAMP/TLR4/AP-1/IL-33 mechanistic pathway was responsible for HCC survival and proliferation [40,48]. This evidence concerns the gene IL33 and hepatocellular carcinoma.