In this study, palmitate-induced lipotoxicity enhanced M1 phenotypes in RAW264.7 monocytes/macrophages and increased VEGFR-3 and Lyve-1 expression, which were inhibited by SAR131675 (VEGFR-3 inhibitor) treatment, suggesting that inhibiting VEGFR-3 signaling can prevent diabetic nephropathy by inhibiting renal lymphangiogenesis mediated through macrophage polarization under lipotoxic conditions (67). The gene discussed is FLT4; the disease is diabetic kidney disease.