(i) We have shown that the knockdown of KDM2B is only partially rescued by the overexpression of EZH2, suggesting that KDM2B functions not only by upregulating EZH2, but also by promoting additional pro-oncogenic activities;12 (ii) although the knockdown of EZH2 has profound effects on the viability and the proliferation of human and canine bladder cancer cell lines with few cells surviving beyond 3 days after selection, the robust inhibition of its histone methyltransferase activity by GSK343 (ref. 46) does not (Foltopoulou and McNiel Data not shown). This evidence concerns the gene PRDM9 and urinary bladder cancer.