Although tenascin, fibronectin and type I collagen participate on the tumoral modulation of the “hybrid lesion” follicular and desmoplastic ameloblastoma, the biologic mechanism of desmoplasia calls to newer investigations regarding the other extracellular matrix components, as well as other study methods, in an attempt to understand the conspicuous stromal collagenization and its relationship with the epithelial component of the lesion. This evidence concerns the gene TNC and ameloblastoma.