  At first blush, this seems a vivid case of a homeostatic property cluster kind. However, demarcating mechanisms is far from straightforward. Where we take a mechanism to begin and end is in large part a pragmatic matter (Craver 2009); so, depending upon how we carve up the “homeostatic mechanisms for” cancer, we can yield many or few cancer subtypes. As perhaps may have been expected, Hanahan and Weinberg’s initial picture has been complicated since 2001. In 2011, Hanahan and Weinberg updated their hallmarks to include four more: “genome instability, which generates the genetic diversity that expedites their acquisition, and inflammation, which fosters multiple hallmark functions… reprogramming of energy metabolism, and evading immune destruction.” And, “In addition to cancer cells, tumors exhibit another dimension of complexity: they contain a repertoire of recruited, ostensibly normal cells that contribute to the acquisition of hallmark traits by creating the tumor microenvironment” (2011, 646). In other words, hallmarks of cancer appear to no longer involve all and only intrinsic properties of cancer cells, but also dynamic interactions between cancer cells and the immune system and extra-tumor environment. This may not be such a serious challenge to Khalidi’s view that caretaker mutation are mechanisms for cancer; one could, arguably, just expand the mechanisms for homeostasis to the tumor microenvironment. However, such a strategy is complicated by the context-sensitivity of mechanism activation. Many cells on the surface of the skin as we age possess as many mutations to “caretaker” genes as those in a breast tumor, but most such skin cells are shed (Martincorena, et al. 2015). The “same” mechanisms may well lead to harm in one context, and be entirely harmless in another.