In parallel, AKT phosphorylation was blocked and vascular endothelial growth factor receptor 3 (VEGFR3) was decreased, suggesting that the regulatory role of hucMSC-Ex in lymphangiogenesis via the miR-302d-3p/VEGFR3/AKT axis mediates amelioration of IBD [138]. This evidence concerns the gene FLT4 and inflammatory bowel disease.