Animal studies corroborate this, with CTLA-4-deficient mice experiencing spontaneous severe myocarditis and pancreatitis, while PD-1-deficient mice develop lupus-like proliferative arthritis and glomerulonephritis on C57BL/6 background and myocarditis on BALB/c background (71, 72, 111). The gene discussed is PDCD1; the disease is myocarditis.