Although fibroblasts decreased tumor necrosis factor (TNF)-α secretion, they were shown to enhance the ability of macrophages to phagocytose bacteria.31 In the same study, gingival fibroblasts, which were called fibroblasts from peri-implantitis inflamed tissues, were at least as active as periodontal ligament fibroblasts in regulating macrophage responses to bacteria.31 Macrophage migration inhibitory factor (MIF) is recognized as a cytokine involved in macrophage and T-cell activation, cell growth, apoptosis, tumor angiogenesis, and carbohydrate metabolism. This evidence concerns the gene MIF and neoplasm.