USP7 and acute myeloid leukemia: Based on all previously identified molecular pathways that are regulated by USP7 (Kim and Sixma, 2017), our own identification of USP7 interaction partners in leukemic K562 cells, and our observation that USP7 is important for PRC1.1 functionality, we propose that the sensitivity of primary AML patient cells toward USP7 inhibition is likely a consequence of interference with USP7 functionality at various molecular levels, which includes PRC1.1 regulation but possibly also other mechanisms, given the diversity of USP7 roles that have now been identified.