In active demyelinating plaques and chronic active and inactive plaques from the brains of MS patients, Clemente et al. [85] described an upregulation of FGF2 in macrophages/microglia, in lesion areas predisposed to remyelination, whereas FGFR1, the receptor of FGF2, was expressed in PDGFRα+ OPCs in chronic active lesions, which the authors suggest could be recruited in response to FGF2. This evidence concerns the gene FGF2 and myeloid sarcoma.