Downregulation of miR-124-3p led to an increase in the level of NRP-1, which in turn played a crucial role in tumorigenesis, invasion, and angiogenesis by interacting with key receptors like class 3semaphorins (SEMA3), vascular endothelial growth factor (VEGF) or transforming growth factor b1 (TGF-B1), ultimately resulting in the repression of tumor angiogenesis and apoptosis in glioma cells, as well as the inhibition of glioma growth upon overexpression of miR-124-3p [38]. The gene discussed is NRP1; the disease is glioma.