Most intriguingly, the overexpression of CCDC32/CBX3 fusion gene in AML patient-specific MV4–11 cells confirms the functional validation, providing experimental evidence of the biological impact of the CCDC32/CBX3 fusion on AML pathogenesis and treatment resistance by promoting cell cycle progression, a mechanism through which AML evolves to become treatment-resistant. Here, CBX3 is linked to acute myeloid leukemia.