The distinction between causal role and selected effect functions is typically framed in terms of their respective explanatory roles. However, much of the controversy over functions in genomics takes place in an investigative, not an explanatory context. Specifically, the process of component-driven functional investigation begins with the designation of some genetic or epigenetic element as functional —i.e. not junk— because it possesses properties that, arguably, suggest some biologically interesting organismal effect. The investigative process then proceeds, in a bottom-up fashion, to (...) search for those effects. I argue that this process encounters a problem reminiscent of one that Gould and Lewontin associated with the adaptationist program. Just as their stereotypical adaptationst became trapped in the myopic pursuit of one selectionist hypothesis after another, so can the investigation of CR functions in genomics lead to an unending series putative organism-level CR functions for junk DNA. This is an acute problem for genomics, because eukaryotic genomes are littered with transposable elements and their deactivated descendants which often masquerade as interesting CR-functional components and it is experimentally onerous to determine whether they lack such a function. I further argue that selectionist reasoning about TE-host coevolutionary dynamics can greatly streamline the investigative process. Importantly, selectionist hypotheses need not be well confirmed to be illuminating in this context. Informed selectionist reasoning about the strategic roles of TEs in the genome offers a corrective to the idea that most of our DNA is somehow CR functional for the organism. (shrink)