Since a number of metabolic pathways are promoted by c-MYC [38,39], and metabolic rewiring is required for development of melanoma and its response to therapy [40], we next investigated the phenomenon of intron retention in a gene of the MCT (monocarboxylate transporter) family (Figure 2), whose critical MCT1 (SLC16A1) gene member is a target and can be directly activated by c-MYC [41,42]. This evidence concerns the gene MYC and melanoma.