Many breast cancer survivors will carry a burden of sequelae after treatments, with pain being one of the most typical symptoms. Aromatase inhibitors (AIs) are the standard endocrine treatment for postmenopausal women with breast cancer diagnoses. Unfortunately, AIs cause painful symptoms, such as musculoskeletal, diffuse, mixed or neuropathic pain, leading to non-adherence or discontinuation of therapy. Although the participation of the TRPA1 channel and kinin B2 receptor (B2R) in AI-induced pain are well characterized, the interaction between these receptors to develop and maintain this painful condition remains unknown. Indeed, the B2R is co-expressed with the TRPA1 channel on sensory neurons, and the downstream signalling pathways from B2R activation, such as the PKC-dependent pathway, is a known intracellular sensitizer of the TRPA1. Thus, downstream pathways activated by B2R could cooperate in sensitizing the TRPA1 channel and sustain the painful symptoms associated with AI use. Here, we reported that the B2R-dependent intracellular signalling pathways PKC seem to interact to sensitize the TRPA1 channel in AI-induced pain.