Animal studies have demonstrated that plasma levels of sFGL2 in BALB/cJ mice were significantly increased after murine hepatitis virus 3 (MHV-3) infection, and treatment with anti-FGL2 antibody or antisense plasmid complementary to the exon 1 of FGL2 gene could protect susceptible BALB/cJ mice against MHV-3-induced fulminant viral hepatitis (FH) and mortality [13, 83]. This evidence concerns the gene FGL2 and familial hyperaldosteronism.