The combination promotes mineralized tissue formation, controls infections, prevents microleakage, and maintains the vitality of pulp.2, 7, 23Dental pulp fibroblasts interact with macrophage and modulate their differentiation into M1 (proinflammatory) macrophage to control infection and M2 (anti-inflammatory) to secrete of growth factor such as TGF-β1, FGF-2, VEGF, and complement proteins (C3a and C5a), allowing dental pulp stem cell migration and odontoblastlike cell differentiation. The gene discussed is VTN; the disease is infection.