We, thus, examined whether macrophage-derived HMGB1 would participate in the CPA-induced CSE upregulation, possibly responsible for the endogenous H2S-mediated, Cav3.2-dependent bladder pain, as it did in the acute pancreatitis-related pain and paclitaxel-induced peripheral neuropathy in our previous studies [8,10]. The gene discussed is HMGB1; the disease is peripheral neuropathy.