Our previous biochemical studies showed that MLN4924 treatment of AML cell lines and de novo AML ex vivo results in inhibition of CRL Neddylation, accumulation of the CRL substrate c‐Myc, and c‐Myc mediated transactivation of the PMAIP gene that encodes the propapoptotic Bcl‐2 family member Noxa [27, 43]. This evidence concerns the gene PMAIP1 and acute myeloid leukemia.