Based on reversible linkage of chemically modified 10058-F4 and 10074-G5 to produce larger molecules, well-suited for targeting the Myc-Max dimer surface and capitalize on the drug-like properties of the small molecule components, Wanner et al. (2015) [107] generated intracellular self-assembly dimeric inhibitors that showed improved potency and activity in cancer cell lines overexpressing Myc (such as Daudi and Raji Burkitt’s lymphoma human cell lines). This evidence concerns the gene MYC and Burkitt lymphoma.