Aromatase inhibitors (AIs) are considered first-line drugs in the endocrine treatment for postmenopausal women diagnosed with breast cancer. However, one-third of users have reported adverse effects from treatment onset. Painful musculoskeletal symptoms, characterized by morning stiffness, joint pain, myalgia, and decreased strength, seem preponderant daily symptoms in these patients. Furthermore, this painful condition can be described as diffuse (22%), mixed (11%), or neuropathic pain (9%). Some mechanisms have been proposed to explain AI-related pain symptoms, including the altered function of ion channels in sensory neurons, such as Transient Potential Receptor Ankyrin 1 (TRPA1) and kinin B1 and B2 receptors (B1R and B2R). However, another of the TRPs family member, vanilloid 4 (TRPV4), is also emerging as one of the primary mediators in several pain models, such as those induced by chemotherapeutic drugs. Furthermore, the PKCε signalling pathways dependent on kinin receptors activation have been previously suggested to be involved in the sensitization of TRPV4 in a model of chemotherapy-induced neuropathic pain. Thus, it is plausible to suggest that kinin receptors and TRPV4 may act together to sustain pain symptoms induced by AIs. Here, we demonstrated the TRPV4 involvement and PKCε signalling pathways downstream from kinin receptors activation and their interaction with TRPV4 in the AI-induced pain model.