Although enhanced presence of MMP7 in active demyelinating MS lesions is well documented (Anthony et al., 1997; Cossins et al., 1997; Lindberg et al. 2001), the persistence of fibronectin (aggregates) in chronic MS lesions suggests that the inability to clear fibronectin is due to the lack of expression and/or impairment of its activity. This evidence concerns the gene FN1 and myeloid sarcoma.