  Given the complex causal pathways and heterogeneity of cancer, perhaps it is not surprising that, as Bertolaso (2016) argues, the history of attempts to identify defining features of cancer, let alone arrive at a unified theory, have floundered. Either cancer is defined so vaguely as to include non-pathological states, or focused so narrowly on a specific class of causes as to rule out cases that might otherwise be included. Among the many definitions she canvases are: “abnormal proliferation,” “unregulated growth,” “a disease of cell differentiation rather than multiplication,” “the result of destruction of tissue architecture,” “a systems biology disease,” “blocked ontogeny,” a disease of “suppressed (sic) immune function,” a “metabolic” and of course, a “genomic” disease. Such a variety of definitions is, Bertolaso argued, due to the fact that cancer has many causes, and many effects; moreover, it involves many different types of dysregulation, at a variety of temporal and spatial scales. Suffice it to say, it is no small challenge to identify defining features of cancer, let alone arriving at a unified “theory” of disease etiology.