Additionally, UBE2N-mediated K63 ubiquitination stabilizes oncogenic protein networks to maintain protein homeostasis in AML, whereas UBE2N inhibition triggers immunoproteasome-dependent K48 ubiquitination and degradation pathways, highlighting the bidirectional regulatory role of immunoproteasomes in AML [168]. Here, UBE2N is linked to acute myeloid leukemia.