FN1 and myeloid sarcoma: Hence, transient Fn expression upon demyelination [15–17] likely contributes to the temporal classical phenotype of microglia and macrophages, whereas in MS lesions Fn persists as aggregates, and as a consequence, microglia and macrophages may retain and/or gain some pro-inflammatory features that may interfere with the regenerative alternatively activated phenotype that is required for remyelination [13].