Other authors suggest different hallmarks, with many papers pointing alternative processes as their primary focus of their research. The difference may stem from the fact that these authors prefer to cite as ''key hallmarks'' physiological changes which occur at a ''lower level'' scale closer to the molecular events. These authors cite, for example, ''mitochondrial dysfunction'' [5, 6] (including, but not limited to ''glucose avidity'' [7] and ''a shift in glucosemetabolism from oxidative phosphorylation to glycolysis'' [6, 8] , ''altered glycolysis'' [9] , ''altered bioenergetic function of mitochondria'' [10] ), ''dysregulation of cell cycle and defective genome-integrity checkpoints'' [11] , ''aberrant DNA methylation'' [12] (''promoter hypermethylation of hallmark cancer genes'' [13] and ''CpG island hypermethylation and global genomic hypomethylation'' [14] ), ''shift in cellular metabolism'' [15, 16, 17] , ''regional hypoxia'' [18] , ''microenviroment acidosis'' [19] , ''abnormal microRNA regulation'' [20, 21] , ''aneuploidy'' and ''chromosome aberrations'' [22, 23, 24, 25, 26] , ''disruption of cellular junctions'' [27] , ''avoidance of the immune response'' [28] , ''pre-existing chronic inflammatory conditions'' [29, 30] , ''cancerrelated inflammation'' [29] , ''disabled autophagy'' [28] , ''impaired cellular senescence'' [31] , ''altered NF-kappaB signalling'' [32] , ''altered growth patterns, not altered growth per se'' [33] , ''disregulated DNA methylation and histone modifications'' [34] , ''tissue dedifferentiation'' [35, 36] , and ''somatically heritable molecular alterations'' [37] . This research enriches the list of the most important cancer hallmarks. However, these physiological changes occur at a ''lower'' molecular level they are likely related sub events of the orginial seven instead of newly discovered ''key hallmarks''. More recently, Luo et al attempted a ''stress-based'' description of some of the hallmarks in terms of ''stresses'' (''DNA damage/replication stress, proteotoxic stress, mitotic stress, metabolic stress, and oxidative stress'') [38] . While this is an interesting descriptive grouping, it is still a phenotypical characterization. What is needed is a higher level unifying genotypical characterization, from which individual disregulated processes can be identified in a quantitative way using the existing high-throughput data capture methodologies. It is clear that a unifying hallmark is needed if we aim at quantifying the cell's progression. It is then evident for us that a unifying mathematical formalism is necessary to uncover the cell transcriptome's progression from a normal to a more malignant phenotype.