To identify the molecular pathways induced by DIO that could drive abnormal endothelial-OPC signaling and thereby impair baseline and post-stroke remyelination, we used a cell-specific RiboTAG approach employing Tie2-Cre:RiboTag and PDGFRα-CreERT2:RiboTag mice to tag ribosomes in endothelia and OPCs, respectively, enabling translating ribosome affinity purification (TRAP)35 (Figure 3A). The gene discussed is TEK; the disease is stroke disorder.