The more usual route, and the one taken both by Sterelny et al. (1996) and by Maynard Smith (2000) is to focus on the natural selection of particular genetic elements. That view faces an immediate problem, for the fact that specific genetic elements (or the genetic system as a whole) have an evolved function is clearly not sufficient for genes to carry semantic information.  Legs are for walking, but they do not represent walking. Enzymes are for catalyzing reactions, but they do not instruct this activity. There are things that legs and enzymes are supposed to do, but this does not make them into information-carriers, in a rich beyond-Shannon sense. Why should it do so for genes? Sterelny, Smith and Dickison (1996), suggested that the differences between genes and legs is that genes have been selected to play a causal role in developmental processes. They add, however, that any non-genetic factors that have a similar developmental role, and have been selected to play that role, also have semantic properties. So Sterelny, Smith and Dickison want to ascribe very rich semantic properties to genes, but not only to genes. Some non-genetic factors have the same status. Even so, many quite plausible cases turn out not to be informational on this view: prolactin, like most hormones, does not have a specifically developmental function, so it would not count as carrying information to the mammary glands. This is one reason why Levy thinks of talk of information as merely metaphorical (Levy 2011). In contrast to the views of Sterelny, Smith and Dickison, in his 2000 paper, John Maynard Smith argued that only genes carry semantic information about phenotypes. He suggested that in contrast to other developmental resources, the relationship between adapted gene and phenotypic outcome is arbitrary; the gene-trait relationship is like the word-object relationship. This idea is intriguing but hard to make precise. One problem is that any causal relation can look “arbitrary” if it operates via many intervening links, for there are many possible interventions on those links which would change the product of the causal chain. The problem of arbitrariness is discussed further in section 4.