The first investigation was conducted on PD-1-deficient animals by Nishimura et al. The exposition of C57BL/6(B6)-PD-1− transgenic mice to Fas mutation results in spontaneously developed lupus-like proliferative arthritis and glomerulonephritis with predominant IgG3 deposition as well as dilated cardiomyopathy with the presence of cardiac troponin I antibodies. This evidence concerns the gene TNNI3 and glomerulonephritis.