  One might well ask, however, whether the lack of a unified theory of cancer is a cause for concern? Is this a sign of immature science? Kincaid has argued to the contrary (2008), “biomedical science can make significant progress without precise definitions of disease, without full-fledged theories of disease and of normal biological functioning, and without disease entities being natural kinds” (p. 368). Pointing out how tumor microenvironment shapes how cancer cells behave as they do, Kincaid argues that “There is no clear definition of what constitutes a cancerous cell in terms of necessary and sufficient conditions. However, no one thinks that cancer research should stop until we get this definition settled, or that creating linguistic uniformity is important for understanding the science. The science certainly makes progress nonetheless… Likewise, there is no parsimonious theory of the disease and the normal functioning from which it is a deviation. Instead, we have piecemeal causal explanations” (p. 373). Kincaid is correct. Much of cancer research is piecemeal in character, offering partial and locally constrained characterizations of the loss or promotion of some particular activity of a cell associated with this or that mutation typical of cancer cells. Whether we require a unified theory of cancer remains an open question. Or, at least, the question of what function such a unified theory might serve is a matter of some debate. This is reflected in the fact that the research program seeking to identify genetic mechanisms associated with cell birth and death has received so many different names: the “oncogene paradigm,” (Bishop 1995; Morange 1997) “vision,” (Morange 1997), “theory,” (Sonnenschein &amp; Soto 2008), “model” (Temin 1974; Vogelstein &amp; Kinzler 1993), “theory-method package” (Fujimura 1988, 1992), and recently, “framework” (Blassime, et al. 2013).