In Schwann cell progenitors, the JAK/STAT pathway is important in autoimmune, and β-catenin regulates the maintenance of stem-like pluripotency, whereas the concurrent loss of NF1 in genetically engineered mouse models leads ultimately to neurofibroma generation and maintenance myeloproliferative disorders, and drugs targeting this pathway are currently used to treat rheumatoid arthritis, ulcerative colitis, and myelodysplastic syndrome. This evidence concerns the gene SOAT1 and neurofibroma.