Though much more research needs to be done, researchers have mostly agreed that a mutation in SOS1, son-of-sevenless gene, is responsible for this disease. SOS1 is a guanine nucleotide-exchange factor that functions in the transduction of signals that control cell growth and differentiation. A mutation in the SOS1 gene results in a single nucleotide insertion. Specific linkage studies have localized the mutation for isolated, nonsyndromic autosomal dominant forms of<unk>  fibromatosis to chromosomes 2 and 5, more specifically 2p21-p22 and 5q13-q22. Genetic<unk> 1 - Caused by a mutation in the SOS1 gene localized on chromosome 2p21-p22<unk> 2 - Caused by a mutation in the SOS1 gene localized on chromosome 5q13-q22 Mutations in the RE1-silencing transcription factor (REST) gene can also cause this syndrome. Non genetic<unk>  may also be caused by unwanted side effects of pharmacological agents like phenytoin, ciclosporin, and some calcium-channel blockers, meaning<unk>  is a disease that can be drug-induced. However, there is little next to no research done in this area to support the claim. * Inflammation * Hormonal Imbalance * Neoplasia * More commonly associated with an autosomal dominant gene inheritance * Multi-system syndromes: Zimmerman-Laband syndrome, Jones syndrome, Ramon syndrome, Rutherford syndrome, juvenile hyaline fibromatosis, systemic infantile hyalinosis, and mannosidosis * Some unknown causes
Hereditary gingival fibromatosis
Connective tissue nevus
Acral fibrokeratoma
Gingival fibromatosis with hypertrichosis
Congenital melanocytic nevus
Basal cell adenoma
Dermal cylindroma
Hydrocarbon keratosis