In addition, studies in a murine model of human focal segmental glomerulosclerosis (FSGS) demonstrated that the number of kidneys CD103+ DCs (cDC1s) is significantly higher in mice with adriamycin nephropathy (AN) than in normal mice, and depletion of CD103+ DCs impairs activation and proliferation of CD8+ T cells and kidney injury. This evidence concerns the gene CD8A and focal segmental glomerulosclerosis.