Mechanistic studies have suggested that the persistent intracranial inflammation in CM is characterized by high levels of T helper 1 (Th1) cell-associated proinflammatory cytokines such as interferon (IFN)-γ, tumor necrosis factor (TNF)-α, granulocyte colony-stimulating factor (G-CSF), and interleukin (IL)-6 in CSF [16, 17]. The gene discussed is CSF3; the disease is cutaneous mastocytosis.