To verify the dynamics of the molecular mechanism and the cancer immune crosstalk, we finally derived a mathematical ordinary differential equation (ODE) model based on the core cancer-immune interaction network that describes the activation of the E2F1-STAT3/IL-6/IL6R signaling pathway and consequences of the interplay between E2F1 and STAT3 on transcriptional regulation of IL-6 (auto- and paracrine activation; Figure 5A). This evidence concerns the gene STAT3 and cancer.