USP7 and acute myeloid leukemia: In particular, disrupting USP7 activity might represent a direct β-catenin-targeting mechanism in AML given USP7’s known regulation of β-catenin stability [146,147], and recent evidence demonstrating that USP7 inhibition (both genetic; siRNA, and pharmacological; P22077) reduces AML cell proliferation and enhances chemosensitivity [148].