Upon UBE2N inhibition, K48-mediated ubiquitination of NPM1 and STAT3 was increased in AML cells treated with ONX-0914, suggesting that loss of UBE2N results in increased K48-linked ubiquitination and degradation of oncoproteins via the immunoproteasome (Figure 5E). This evidence concerns the gene UBE2N and acute myeloid leukemia.