For example, at CSNK1A1, a drug target in acute myeloid leukemia (AML) tumor cells (Järås et al., 2014), VEGFA, which is upregulated in many cancers (Goel and Mercurio, 2013), and RUNX1, a well-defined oncogene in AML (Deltcheva and Nimmo, 2017), the evidence suggests that super-enhancers in these cancer cells use a CTCF enhancer-docking mechanism to interact with the oncogene. Here, RUNX1 is linked to neoplasm.