Canonical Wnt/β-catenin signaling mediates podocyte injury and the development of proteinuria,18, 20 and podocyte-specific deletion of β-catenin protects from nephropathy.19, 20 Tankyrases have been shown to be efficient targets in inhibiting this signaling.17 Here, we show that CD2AP interacts with tankyrase 1 and tankyrase 2, and that in the absence of CD2AP tankyrase-mediated total PARylation in podocytes is increased. The gene discussed is TNKS; the disease is Nephropathy.