Therefore, the effects of select TYRO3 agonists would be podocyte-specific; and (c) we have strong in vivo data supporting a protective role of the PS/TYRO3 signaling axis against podocyte injury in glomerular disease; this is in contrast to the disease-promoting effects of AXL/MER signaling in mesangial cells in DKD (12, 17). This evidence concerns the gene AXL and glomerular disorder.