Examples where such situations might be particularly salient include tumors where high levels of Myc-Max might displace MondoA/ChREBP-Mlx heterodimers from their target genes, particularly when the latter’s binding sites are low-affinity or when the tumor micro-environment is deprived of glucose and/or highly acidic, as commonly occurs when tumor proliferation outpaces the vascular and nutrient supply [9,82] (Figure 2). This evidence concerns the gene MYC and neoplasm.