PD-1–deficient mice develop lupus-like glomerulonephritis as they age, and anti–PD-1 treatment of a murine adriamycin nephropathy model led to worsened glomerular and tubulointerstitial injury, consistent with a role for immune checkpoints in self-tolerance (26, 27). The gene discussed is PDCD1; the disease is systemic lupus erythematosus.