KD was also shown to improve responses to several PI3K inhibitors in tumors with a wide range of genetic aberrations such as in patient-derived xenograft models of advanced endometrial adenocarcinoma (harboring a PTEN deletion and PIK3CA mutation), bladder cancer (FGFR-amplified), in syngeneic allograft models of PIK3CA mutant breast cancer and in a MLL-AF9 driven acute myeloid leukemia. This evidence concerns the gene KMT2A and urinary bladder carcinoma.