A couple of reviewers of WEIT (and some of my friends and colleagues) have pointed out the book’s dearth of molecular evidence for evolution. For example, why didn’t I stress that organisms thought to be related based on morphological similarities also show similar relationships in their DNA sequences? That is, DNA phylogenies generally match morphologically-based phylogenies — doesn’t that count as evidence for evolution? To my mind, not very strongly, and for two reasons. First, at least for protein-coding genes, morphology and DNA are not independent: the genes are blueprints for the organism’s appearance, so the coincidence of trees is not independent evidence for evolution.
My strategy here was to use as evidence for evolution only those data that rule out the most widely-accepted alternative scenario, i.e., some form of creationism. Similarities of molecular and morphological trees don’t necessarily rule out the action of a celestial designer. He/She/It could have used similar genes to make similar organisms.
Well, you ask, what about those parts of the DNA that are “neutral”? (E.g., the third positions of codons, in which a mutation doesn’t necessarily change the structure of the protein made by that gene.) Well, yes, those could count provided that they really are neutral. As molecular evolutionists examine genomes more thoroughly, they often find that “neutral positions” aren’t really neutral, but could play some role in the fitness of the organism. In such cases, their phylogenetic match to appearance-based phylogenies again fails to rule out creationism.
The one type of molecular evidence that does absolutely rule out creationism, I think, involves pseudogenes: those genes that were once active in ancestors but have become inactivated. I describe several cases in chapter 3 of WEIT; they include olfactory receptor genes in humans, many of which have become inactivated in the human lineage as we gradually lost reliance on our sense of smell and became more vision-oriented. DNA changes in pseudogenes can hardly be subject to natural selection, so pseudogenes change in a purely time-dependent manner as those dead genes accumulate mutations over time. Thus, the match between phylogenetic trees based on pseudogene DNA sequences (reflecting only the passage of time) with phylogenetic trees based on organisms’ appearance are expected under an evolutionary scenario but not a creationist one. Creationists largely deny common ancestry (and don’t accept that organisms change with the passage of time). They wouldn’t, then, predict a phylogenetic match between features that simply mark the passage of time and features that independently reflect ancestry (e.g., the placenta of placental mammals that is not found in marsupials). This is why I concentrated on pseudogenes in my book. I’ve never seen a creationist explanation for why DNA trees based on pseudogenes match traditional trees based on morphology.
Similarly, people often cite Hox (“homeobox”) genes as evidence for evolution (these are the genes that demarcate different segments of animal bodies). It turns out that in organisms which are very dissimilar, such as humans and my beloved fruit flies, Hox genes nevertheless play similar roles in building bodies. Why don’t I count this as evidence for evolution? Because it doesn’t rule out the alternative of a celestial designer. Such a designer could have used the same genes in different species as His/Her/Its way of building bodies. There’s no reason why a designer couldn’t hit on certain fundamental ways of making bodies, and then use them over and over again.
This, then, was my strategy throughout the entire book: to use only that evidence that could not easily be explained by creationism or other alternatives to evolutionary theory. This, of course, is precisely the strategy that Darwin used in The Origin, since he had to convince readers that his theory was superior to the reigning creationist paradigm of the day. I guess you can say that, given prevailing opinions in the US and some other countries, I adopted the same evidence-based strategy.