Therapeutic targeting of APL by all-trans retinoic acid and/or arsenic trioxide (ATO) results in the proteasomal degradation of PML::RARA and restoration of tumor-suppressive PML bodies.76 Similarly, the neddylation inhibitor MLN4924 neutralized enhanced chromatin binding of PML::RARA, leading to the reformation of physiological PML bodies80 (Figure 3D). The gene discussed is PML; the disease is neoplasm.