In exploring therapeutic options for targeting PRC1, BMI1 was uncovered as an attractive target when Rizo et al. discovered that knocking down BMI1 impairs the self-renewal capacity of leukemic stem cells.99 Additionally, Shima et al. have shown that RING1A/B activity is necessary for leukemogenesis and disease progression in mouse models of AML.88 To this end, Shukla et al. sought to design small molecule inhibitors targeting PRC1. The gene discussed is BMI1; the disease is acute myeloid leukemia.