The overall effect induced by sildenafil that emerged in the MS experimental models can be described as a significant downregulation of the subset T helpers, (Th)1 (CD4+), which are critical for disease initiation and maintenance, and Th17, which are the main cells responsible for persistent inflammation and are the source of IL-17 which is highly expressed in blood, cerebrospinal fluid and local CNS lesions in MS patients [53,54,55,56,57]. The gene discussed is CD4; the disease is myeloid sarcoma.