For further evaluation whether neuroprotective effects we observed in therapeutic treatment of chronic EAE could be translated from the mouse model to siponimod treatment effects in SPMS, we analyzed the expression of serum NfL (sNfL), a biomarker for neuroaxonal damage, and of serum GFAP (sGFAP) as surrogate marker for progression in our MS patient cohorts and their age-matched healthy controls with a SIMOA multiplex assay (Supplementary Fig. 5). This evidence concerns the gene GFAP and myeloid sarcoma.