Regarding the role of 2-AG in the bladder and its opposite pattern to AEA, reduced inflammation in CB1R antagonist-treated mice may be due to the recovery of 2-AG (preferential a CB2R ligand) levels, and it may support the anti-inflammatory role of CB2R that was well established in cystitis.25,26 Since we have not measured the protein expression of CB2R (due to lack of a valid antibody), we cannot comment further on its role in our settings. This evidence concerns the gene CNR1 and chronic cystitis.