The addition of sodium thiosulfate (STS), an H2S donor, effectively alleviated D-galactosamine (GalN)- and lipopolysaccharide (LPS)-induced acute liver failure in the wild-type mice by activating Akt- and Nrf2-dependent signaling and by inhibiting GalN/LPS-induced JNK phosphorylation. This evidence concerns the gene GAL and acute liver failure.