To this end, we characterized the expression of Raldh2 in microglia/macrophages and OPCs in active lesions (site of ongoing demyelination and early-stage repair), perilesions (site of later stage repair), chronic inactive lesions (site of failed repair), and normal appearing white matter (NAWM) from postmortem MS brain sections (Figure 8A). This evidence concerns the gene ALDH1A2 and myeloid sarcoma.