CX‐5461 treatment could effectively inhibit mouse MLL‐fusion AML progression and human AML cell lines in both Trp53‐dependent and ‐independent mechanisms.[50, 51] Also, combination therapy targeting ribosome biogenesis and mTORC1‐dependent translation synergistically extends survival in MYC‐driven lymphoma.[52] Thus, several phase I clinical trials of CX‐5461 in B‐cell lymphomas and solid cancers have been done[53] or are ongoing (NCT02719977, NCT04890613, and NCT05425862). The gene discussed is KMT2A; the disease is B-cell non-Hodgkin lymphoma.