Researchers suggested that miR-486-5p’s anti-fibrotic effects in DKD were due to its targeting of NFAT5 [29], a protein that plays a pathogenic role in the disease by increasing the activity of nuclear factor (NF)-κB, which in turn promotes the expression of genes related to angiogenesis, platelet activation, vascular smooth muscle cell and macrophage migration, and pro-inflammatory cytokine expression [30]. The gene discussed is NFKB1; the disease is diabetic kidney disease.