Fibroblasts and mast cells are key players in the promotion of tumor growth in the neurofibroma microenvironment, as well as in wound healing and scar formation.1, 2 As previously reported, the activation of IL-4 and IL-13 pathways in fibroblasts, mediated by JAK/STAT intracellular signaling, leads to excessive collagen production, which is responsible for neurofibroma development.3 The gene discussed is SOAT1; the disease is neurofibroma.