Treatment of acute myeloid leukemia (AML) cells with dBET1 induced highly selective cereblon-dependent protein degradation of BET family members in vitro and in vivo, resulted in transcriptional downregulation of MYC, induction of antiproliferative responses in leukemia cells in vitro and delayed proliferation and leukemia progression in mice, without toxicity, thus underscoring the potential clinical utility of this approach [412]. The gene discussed is CRBN; the disease is acute myeloid leukemia.