Tumor dormancy during equilibrium implies that the tumor cells have “survived” the elimination phase but their progression is successfully restrained by immune-mediated mechanisms reflecting activation of Th1-associated factors such as IFN-γ, STAT1, IRF1, IL-12 as well as upregulation of CD8 genes and chemokine receptor pathways (CXCR3/CXCL9–11 and CCR5/CCL3–5) [2,33,65]. The gene discussed is CXCL9; the disease is neoplasm.