These features, the presence of CTCF sites in tumor super-enhancers, and the ability of two CTCF-bound sites to be brought together through CTCF homodimerization (Saldaña-Meyer et al., 2014; Yusufzai et al., 2004) led us to further study the possibility that the −2 kb site has an enhancer-docking function critical to MYC expression. Here, MYC is linked to neoplasm.