Treatment for joint pain in rheumatoid arthritis (RA) continues to be a challenge and represents a large unmet medical need. Although RA pain is often thought to result from inflammation, it often persists even after optimal control of inflammation with currently available therapies, indicating the involvements of other non-inflammatory mechanisms. Our lab is exploring the potential inflammation-independent mechanisms of RA pain using mouse genetics and behavioral/physiological approaches. Moreover, to visualize and analyze the alterations of the activity of joint sensory neurons, we recently developed two powerful approaches, including in vivo dorsal root ganglion (DRG) neuron imaging and in vivo electrophysiological recordings on the intact DRG. The long-term goal of my research is to illuminate a novel peripheral neural mechanism underlying RA pain independent of joint inflammation and define a promising therapeutic target for RA pain that is resistant to current anti-inflammatory treatments or occurs in patients for whom such treatments are infeasible or poorly tolerated.