Because of the apparent importance of GM-CSF and IL-3 for CNS autoimmunity, their deregulation in MS-patients (44, 57, 59, 60), their functional relationship (47, 48, 55) and the correlation of Cbl-b with autoimmunity as well as the hyper-responsive Cblb−/− T cell phenotype (1–3, 17–19), we were interested to find out whether Cbl-b suppresses EAE through the regulation of GM-CSF and IL-3. This evidence concerns the gene IL3 and myeloid sarcoma.