This mechanism also predicts additional venues in which single agent WINi activity may be expected, such as Burkitt lymphomas expressing mutant forms of MYC—which typically retain wild-type p53 [87]—as well as the large fraction of “MYC-driven” cancers (e.g., diffuse large B-cell lymphoma) that preserve p53 function on a case-by-case basis [88]. This evidence concerns the gene TP53 and Burkitt lymphoma.