ABSTRACT Hibernation is a powerful response of a number of mammalian species to reduce energy during the cold winter season, when food is scarce. Mammalian hibernators survive winter by spending most of the time in a state of torpor, where basal metabolic rate is strongly suppressed and body temperature comes closer to ambient temperature. These torpor bouts are regularly interrupted by short arousals, where metabolic rate and body temperature spontaneously return to normal levels. The mechanisms underlying these changes, and in particular the strong metabolic suppression of torpor, have long remained elusive. As summarized in this Commentary, increasing evidence points to a potential key role for hydrogen sulfide (H 2 S) in the suppression of mitochondrial respiration during torpor. The idea that H 2 S could be involved in hibernation originated in some early studies, where exogenous H 2 S gas was found to induce a torpor-like state in mice, and despite some controversy, the idea persisted. H 2 S is a widespread signaling molecule capable of inhibiting mitochondrial respiration in vitro and studies found significant in vivo changes in endogenous H 2 S metabolites associated with hibernation or torpor. Along with increased expression of H 2 S-synthesizing enzymes during torpor, H 2 S degradation catalyzed by the mitochondrial sulfide:quinone oxidoreductase (SQR) appears to have a key role in controlling H 2 S availability for inhibiting respiration. Specifically, in thirteen-lined squirrels, SQR is highly expressed and inhibited in torpor, possibly by acetylation, thereby limiting H 2 S oxidation and causing inhibition of respiration. H 2 S may also control other aspects associated with hibernation, such as synthesis of antioxidant enzymes and of SQR itself.