Our previous and current data thus indicate that TYRO3 agonism may offer a new therapeutic avenue, based on these key findings: (a) TYRO3 expression negatively correlates with the progression of human glomerular disease, supporting a critical role of TYRO3 in kidney disease in humans (17); (b) single-cell transcriptomic data indicate that TYRO3 expression in the kidney is limited to podocytes, with relatively low expression in macrophages when compared with AXL and MER. This evidence concerns the gene AXL and glomerular disorder.