In the 1970s Gresser and colleagues [17] were the firsts to suggested the existence of possible pathogenic effects of IFN: newborn animals injected with high doses of IFN presented the same severe growth retardation, liver lesions, glomerulonephritis and mortality of animals infected by lymphocytic choriomeningitis virus (LCMV) suggesting that IFN itself was responsible for the induction of those lesions. This evidence concerns the gene IFNA1 and glomerulonephritis.