TGF-β, widely recognized as a regulator of the ECM, is associated with fibrosis in various diseases.42 TGF-β1 levels in GCF of patients with drug-induced GO have been suggested as a possible indicator of GO.43 Research in animal models of fibrosis indicates that the CX3CL1–CX3CR1 signaling pathway directly influences collagen production.13,44 Shimizu, et al.44 (2011) demonstrated that the CX3CL1–CX3CR1 pathway contributes to renal fibrosis in a mouse model of hypertension, likely by promoting macrophage infiltration and increasing TGF-β1 and type I collagen expression. Here, TGFB1 is linked to hypertensive disorder.