Consistent with the vast literature on c-Myc's role in genesis of many cancers (Dang, 2012), predictions indicated that c-Myc linked multiple pathways such as ERK and PI3K/AKT to regulation of cell cycle arrest (Table 1; also see Figure 6—figure supplement 2 for the highly complex c-Myc response to targeted perturbations in the underlying RPPA data). This evidence concerns the gene MYC and cancer.