Fig. (2) Diagram Summary. The figure shows a simplified schematic model, which is applicable to all the inducing drugs, although the predominance of the pathogenic mechanisms described may vary.The gingival tissue is subjected to multiple aggressions that induce a state of permanent tissue repair involving the inflammatory cells, fibroblasts and chemotactic factors. The presence of myofibroblasts is a well-established feature of the wound healing process.Genetically predetermined gingival fibroblasts -responders- are more sensitive to the GO-inducing drugs than other fibroblast subpopulations. This fibroblast heterogeneity leads to variations in the production of potentially proliferative, fibroblastic cytokines/GFs, and in their environmental responses to ECM components; myofibroblast cell possesses profibrotic characteristics capable of synthesizing molecule compounds for tissue remodeling, as observed in DIGO. The myofibroblast is active during the reparative process of DIGO, but disappears selectively due to apoptosis and the survival of other fibroblasts groups. Myofibroblast apoptosis is critical for normal healing, as the persistence of cell favors continuous ECM deposition and the development of pathologic fibrotic conditionsDIGO – Drug Induced Gingival OvergrowthSOS-1 – Genetic variability of fibroblasts with phenotypes of different behavior (Integrin function modulation)(*) Genetic risk factor for DIGO.