In our work, in the effort to investigate and understand MS etiology, we focused on five genes related to the pro-inflammatory NF-κB signaling pathway (i.e., CCL2, NFKB1, MAPK14, TNFRSF1A, CXCL10), given the observation that this pathway is out of balance in MS and could represent a valid therapeutic target via inhibiting proper molecules implicated in it. The gene discussed is CCL2; the disease is myeloid sarcoma.