Decreases in the ratios of angiopoietin-1 (ANGPT1) and ANGPT2, abnormal podocyte expression of vascular endothelial growth factor (VEGF), and podocyte/endothelial cell-derived ET-1 induce abnormal angiogenesis by promoting the proliferation and migration of ECs, together with tube formation.50 Furthermore, abnormal VEGF levels impair angiogenesis and lymphangiogenesis, contributing to renal vascular dysfunction,51 whereas lymphatic dysfunction exacerbates interstitial edema and fibrosis.52 The gene discussed is VEGFA; the disease is fibrosis.