For examples, loss of KDM6A amplified PRC2-regulated transcriptional repression of IGFBP3 in urothelial bladder cancer and promoted tumor growth, and sensitized bladder cancer cells and tumors to EZH2 inhibition [124]; moreover, loss of KDM6A led to malignant phenotype in multiple myeloma via deactivating the expression of multiple genes including IRG4 and c-MYC, and EZH2 inhibitors performed better anti-tumor effects in KDM6A loss cases by rebalancing H3K27me3 levels at specific genes [125]. This evidence concerns the gene MYC and neoplasm.