  On this view, cancer is a both a process and byproduct of multi-level selection, where selection may be understood as operating at several levels of biological organization simultaneously, or sequentially (Damuth, et al. 1988; Lean, et al. 2016). That is, cancer cells may bear adaptations, and, they are also evolutionary byproducts of selective processes at other level of organization. It appears that cancer cells co-opt or hijack otherwise adaptive features of organisms. Signaling pathways that are ordinarily in service of adaptive functions in early stages of development or wound healing are reactivated in (some) cancer cells, in service of the transition to metastasis. This is a classic example of a cross-level selective byproduct (Okasha 2005, 2006). Traits advantageous at one level in the organization of multicellular organisms may be coopted by component parts. Some of the capacities that invasive cancer cells acquire (the capacity to invade and metastasize) are in fact due to a change in phenotype from epithelial to mesenchymal type cells, and losing adhesive properties enables such cells to invade the lymph and blood system. Lean and Plutynski (2016) have argued that cancer may in some ways parallel the patterns of emergence of multicellularity as characterized by Damuth and Heisler (1988), shifting over the course of emergence of disease from a simple selective process between individual cells to several kinds of multilevel selective process (MLS1 to MLS2). Critics contest that the process of metastasis only weakly mimics MLS2, however (Germain, et al. 2017).