Despite the pervasiveness of chronic pain worldwide, few effective strategies for long-term pain management exist. The development of new, non-addictive pain interventions hinges upon a deeper understanding of the changes in neural activity and circuitry that drive the development of chronic pain states. Recent studies have implicated the basolateral amygdala (BLA) as a critical hub in the encoding of negative valence to nociceptive information. Using immediate early gene mapping in combination with an activity-based rabies viral tracing screen, we identified several brain regions that synapse directly onto the BLA nociceptive ensemble and exhibit increased labeling during the chronic pain state, which is indicative of persistently elevated levels of activity that correspond to elevated intrinsic excitability. Notably, the agranular insular cortex (AIC) emerged as a sensitized input region, suggesting its involvement in pain processing. To elucidate the functional role of the AIC→BLA circuit in pain modulation, we employed an intersectional genetic approach to selectively silence these projection neurons. Inhibition of AIC→BLA neurons prior to chronic pain-inducing injuries effectively blocked the development of mechanical hypersensitivity, highlighting its crucial role in pain chronification. Further investigations are underway to dissect the molecular, genetic, and physiological underpinnings of the larger connected pathways involving the AIC and BLA. Our findings underscore the significance of the AIC→BLA circuit in modulating pain sensitivity and provide insights into potential therapeutic targets for chronic pain.