To identify potential therapeutic targets to treat bladder pain in IC/BPS patients, we have been studying the mechanisms underlying bladder pain in a cyclophosphamide (CPA)-induced cystitis mouse model, and have shown the two different mechanisms involved in the cystitis-related bladder pain, i.e., the activation of the receptor for advanced glycation end products (RAGE) by high mobility group box 1 (HMGB1) [2], and the elevated Cav3.2 T-type Ca2+ channel activity by H2S generated by upregulated cystathionine-γ-lyase (CSE) [3]. Here, AGER is linked to cystitis.