Having demonstrated ARID1A protein loss in a significant portion (10%) of high-grade urothelial bladder carcinomas of different stages including CIS, we analyzed for the first time if a functionally antagonistic relationship between ARID1A and EZH2 exists in urothelial cells, and secondly if inhibition of EZH2 methyltransferase activity could be a potential therapeutic option for ARID1A-deficient bladder carcinomas. This evidence concerns the gene ARID1A and in situ carcinoma.