Multimodal integration is imperative for an organism to form a coherent representation of its environment to select the appropriate behavior. In multisensory integration, one sensory modality can influence the processing of another. One example of cross-processing of sensory modalities is predator odor-induced analgesia, a type of stress-induced analgesia (SIA). In this model, the predator odor induces a high stress state, and mice subsequently display decreased nociceptive responses, a readout of analgesia. While SIA has been shown to critically depend on the central amygdala (CeA), the circuit mechanisms that underlie the way in which specific odor stimuli modulate pain perception remains unknown. Here we show that the predator odor, 2MT, has an analgesic effect in naïve mice. We confirm that 2MT activates a region of the olfactory pathway called the amygdala-piriform transition zone (AmPir), which was previously reported to mediate the stress response to predator odor (Kondoh et al., 2016). We now show that AmPir sends strong projections to a subpopulation of CeA neurons that are activated by general anesthetics (CeA_GA), which have been shown to produce robust analgesia when optogenetically stimulated (Hua et al., 2020). Finally, using both in vivo calcium imaging and cFos expression, we show that CeA_GA neurons are activated by 2MT. Thus, we hypothesize that 2MT produces analgesia by activating AmPir neurons which, in turn, activates CeA_GA. Future studies aim at dissecting the necessity of the AmPir-CeA circuit in predator-induced analgesia through silencing of CeA_GA during exposure to 2MT. These findings will provide novel insights into the neural circuits mediating the interplay between olfaction and pain perception, and advance our understandings of how sensory modalities modulate one another.