Patients with acute lymphoblastic leukemia (ALL) have an inherently intense, dysregulated inflammatory state characterized by Th1 polarization, with higher levels of TNF-α, IL-6, IL-8, monocyte chemotactic protein-1 (MCP-1), and IL-10 in patients with ALL compared to controls (Pérez-Figueroa et al., 2016). This evidence concerns the gene CCL2 and acute lymphoblastic leukemia.