DI-591, a high-affinity, cell-permeable small-molecule inhibitor that effectively blocks the interaction between DCN1 and UBE2M, selectively transforms cellular CUL3 into an un-neddylated, inactive form, with minimal or no effect on other cullin family members, contributing to a dose-dependent accumulation of NRF2 across various cancer cell lines [127]. This evidence concerns the gene UBE2M and cancer.