We therefore posit that the genetic variant in KREMEN2 might contribute to the HGF presentation in this family via exacerbating the already perturbed endosome trafficking as a result of the heterozygous TBC1D2B variant, leading to an increased epithelial-to-mesenchymal transition, uncontrolled cell growth, and subsequent gingival hyperplasia and fibromatosis. The gene discussed is HGF; the disease is fibromatosis.