The proteomics evaluation in a very interesting study, however, showed that the members of the RAAS are upregulated in MS lesions; however, the blockade of these molecules (e.g., with angiotensin-converting enzyme (ACE) inhibitors) suppresses autoreactive Th1 and Th17 cells in EAE mice [114]. The gene discussed is ACE; the disease is myeloid sarcoma.