One of the most appealing, but potentially problematic, features of the idea that genes code for amino acid sequences concerns the alleged “arbitrariness” of the genetic code. The notion of arbitrariness figures in other discussions of genetic information as well (Maynard Smith 2000; Sarkar 2003; Stegmann 2004). It is common to say that the standard genetic code has arbitrary features, as many other mappings between DNA base triplets and amino acids would be biologically possible, if there were compensating changes in the machinery by which “translation” of the genetic message is achieved. Francis Crick suggested that the structure of the genetic code should be seen as a “frozen accident”, one that was initially highly contingent but is now very hard for evolution to change (Crick 1958). But the very idea of arbitrariness, and the hypothesis of a frozen accident, have become problematic. For one thing, as noted in our discussion of Bergstrom and Rosvall (2011) above, the code is not arbitrary in the sense that many others would work as well. To the contrary, the existing code is near-optimal for minimising error costs. Conceptually, it seems that any causal relation can look “arbitrary” if it operates via many intervening links. There is nothing “arbitrary” about the mechanisms by which each molecular binding event occurs. What makes the code seem arbitrary is the fact that the mapping between base triplets and amino acids is mediated by a causal chain with a number of intervening links (especially involving “transfer RNA” molecules, and enzymes that bind amino acids to these intervening molecules). Because we often focus on the “long-distance” connection between DNA and protein, the causal relation appears arbitrary. If we focused on steps in any other biological cascade that are separated by three or four intervening links, the causal relation would look just as “arbitrary”. So the very idea of arbitrariness is elusive. And empirically, the standard genetic code is turning out to have more systematic and non-accidental structure than people had once supposed (Knight, Freeland, and Landweber 1999). The notion of arbitrariness has also been used in discussions of the links between genes and phenotypes in a more general sense. Kirscher and Gerhart (2005) discuss a kind of arbitrariness that derives from the details of protein molecules and their relation to gene regulation. Proteins that regulate gene action tend to have distinct binding sites, which evolution can change independently. To bind, a protein must be able to attach to a site, but that requires congruence only with a local feature of the protein, not sharply constraining its overall shape (Planer 2014). This gives rise to a huge range of possible processes of gene regulation. So there is a perennial temptation to appeal to the idea of arbitrariness when discussing the alleged informational nature of some biological causation.