  Khalidi (2013) argues that cancer might be a homeostatic property cluster kind. Khalidi argues that cancer is driven by “homeostatic” mechanisms—namely, mutations to “caretaker” genes, or genes that play a “gatekeeping” role in preventing or permitting the emergence of a tumor. Acquisition of mutations to specific “caretaker” genes, on this view, serve a function akin to Boyd’s (1999) “homeostatic mechanisms,” in that they permit the further acquisition of “hallmark” properties of cancer cells. Khalidi is drawing upon a very common view of cancer, articulated by two famous cancer researchers, Hanahan and Weinberg (2000, 2011). They identify what they take to be the “hallmarks” of cancer: “a small number of molecular, biochemical, and cellular traits—acquired capabilities—shared by most and perhaps all types of human cancer.” They identified these “six essential alterations in cell physiology that collectively dictate malignant growth” as: self-sufficiency in growth signals, insensitivity to antigrowth signals, evasion of apoptosis (cell death), sustained angiogenesis (the ability to develop a blood supply), tissue invasion and metastasis (Hanahan, et al. 2000, 57). By way of example of a caretaker, TP53 is called a tumor suppressor, because it carries the function of sensing and responding to signals associated with cell damage, typically inducing apoptosis, or cell death. It is one of the only genes mutated in a majority of cancers sequenced (Bailey, et al. 2018), and Weinberg (2013) characterizes it as “master guardian and executioner,” in that it prevents further mutations by inducing cell death where there are signs of trouble. On Khalidi’s view, one ought to understand disruption of these very specific capacities as a “homeostatic mechanism” for cancer.