However, UBE2J2/UBE2K DKO was not able to upregulate the downstream substrates or induce the defective growth of AML in the absence of venetoclax to the same degree as MARCH5 depletion (Fig. 1j, k and Supplementary Fig. 1d), indicating that MARCH5 may collaborate with additional E2s to compensate for the loss of UBE2J2 and UBE2K. Here, UBE2J2 is linked to acute myeloid leukemia.