In mouse model of MS, ChP epithelial cells increase adhesion molecules including intercellular adhesion molecule (ICAM-1), vascular cell adhesion molecule (VCAM-1) and chemokines that induce the influx of pro-inflammatory lymphocytes into the ventricular space: a function probably aided by the established capacity of leptin to increase Th1 and Th17 differentiation and suppress regulatory T (Treg) cells function [85]. The gene discussed is LEP; the disease is myeloid sarcoma.