From the aspect of results of these two distinct mutation types, the gain-of-function of these bladder cancer specific mutations activating GATA4 and ETS1 seem like the translocation and rearrangement alterations from leukemia in which the MLL truncation and fusion proteins activated the transcription of target genes such as Hox genes and induced cell transformation. Here, KMT2A is linked to urinary bladder carcinoma.