As a consequence, we might hypothesize that during inflammatory lesion formation in MS and concomitant deposition of ECM proteins, astrocyte-derived TG2, only in the presence of infiltrating leukocytes or their derived factors, can increase the formation of fibronectin fibril-like deposits which aggregate and may contribute to the process of scarring and subsequent impaired remyelination. Here, TGM2 is linked to myeloid sarcoma.