Further experimental data are essential to study the modulation of the podocyte Ampk signaling axis by established circulating mediators of CKD and podocyte injury, such as SUPAR (57, 58), TGF-β (9, 59), and TNF-α (60, 61) that could then link podocytopenia, glomerulomegaly, and progressive disease with Ampk signaling in each of these instances. This evidence concerns the gene TNF and chronic kidney disease.