Editor’s note: For the full “Chimps and Critics” series by Dr. Luskin, see here.

We’ve been discussing arguments from critics in response to evidence from the new Nature paper showing that humans and chimps are about 15 percent genetically different. The first objection is that the gap divergence simply represents “technical failures” and not real differences. But this is based upon a misreading of the paper — those technical failures derive directly from an inability to align the DNA due to real genetic differences between human and chimp DNA. 

But probably the most common argument I’m seeing against this new dataset seeks to dismiss much of the different DNA between humans and chimps that cannot align because it is claimed to be junk DNA. The critics claim that it merely represents different numbers of copies of repetitive DNA — what they call “meaningless” junk DNA that doesn’t encode “true biological differences” between humans and chimps. 

Already Answered This Objection

I predicted that this was how critics would respond, and already pre-emptively addressed the objection in a previous post. But we’ll dive into it one more time. My previous post noted that a new paper in Nucleic Acids Research — published by some of the same researchers involved with sequencing these new complete ape genomes — studied the precise repetitive DNA that is different between humans and chimps. They found that much of this repetitive DNA can have important functions. I strongly recommend reading this paper because it overturns the assumption many critics are making that you can just ignore non-alignable sections of repetitive DNA. 

The Nucleic Acids Research paper notes that this newly sequenced repetitive DNA can perform a myriad of functions, including structural roles as “non-B” DNA, which is known to be “important regulators of cellular processes” and has “unequivocal importance for genome function.” The abstract discusses the importance of some of these functions:

Non-canonical (non-B) DNA structures — e.g. bent DNA, hairpins, G-quadruplexes (G4s), Z-DNA, etc. — which form at certain sequence motifs (e.g. A-phased repeats, inverted repeats, etc.), have emerged as important regulators of cellular processes and drivers of genome evolution. Yet, they have been understudied due to their repetitive nature and potentially inaccurate sequences generated with short-read technologies. Here we comprehensively characterize such motifs in the long-read telomere-to-telomere (T2T) genomes of human, bonobo, chimpanzee, gorilla, Bornean orangutan, Sumatran orangutan, and siamang. Non-B DNA motifs are enriched at the genomic regions added to T2T assemblies and occupy 9%–15%, 9%–11%, and 12%–38% of autosomes and chromosomes X and Y, respectively. G4s and Z-DNA are enriched at promoters and enhancers, as well as at origins of replication. Repetitive sequences harbor more non-B DNA motifs than non-repetitive sequences, especially in the short arms of acrocentric chromosomes. Most centromeres and / or their flanking regions are enriched in at least one non-B DNA motif type, consistent with a potential role of non-B structures in determining centromeres. Our results highlight the uneven distribution of predicted non-B DNA structures across ape genomes and suggest their novel functions in previously inaccessible genomic regions.

Crucially, the number of copies of repeats helps determine the shape of this non-B DNA which can have implications for genomic interactions and the three-dimensional structure of chromosomes in the nucleus. So we can’t just dismiss any of these DNA differences simply because they pop up as different copy numbers of repetitive DNA. Those different copy numbers can entail meaningful functional differences. 

Indeed, a 2025 paper in Nature Communications noted that changes in shapes of DNA (e.g., DNA loops) can lead to changes in gene regulation, which is crucial for genome function: 

The major genetic differences between humans and these primates reside in the non-coding regions of the genome. It is postulated that alterations in gene regulation serve as a driving force for evolutionary innovation during speciation. … An increasingly important dimension to this enigma is that the spatial organization of the genome within the nucleus plays a central role in determining which genes are accessible for transcription and which remain dormant. In the three-dimensional (3D) genome, regulatory landscapes are partitioned into preferentially self-insulated domains where enhancers communicate with promoters. Changes in the 3D genome architecture can have cascading effects, rewiring gene regulatory networks and potentially resulting in various diseases. 

In short, differences in the number of copies of repeat sequences can affect the size and shape of DNA loops and the 3D shape of chromosomes, which in turn can influence transcription factor binding, gene expression, and other genome functions. We can’t just dismiss these kinds of repeat differences as junk. 

Dismissing the Differences

Despite this evidence, some critics dismiss the repetitive DNA as junk. On X, Christian biologist Joshua Swamidass, who defends human-chimp common ancestry, argued that a large portion of human DNA that doesn’t align with chimp is “repetitive satellite DNA” that “contributes to the total gap-divergence.” He calls it “trivial” because it represents mere “cut-and-paste repetitions.” Here’s the full text of the tweet:

See this portion of chromosome 16. The large pink block doesn’t align to chimps but it is just repetitive satellite DNA in Humans. So it contributes to the total gap-divergence, even though it’s trivial cut-and-paste repetitions. More interesting and important is the divergence of the blue and yellow sections, the ‘aligned’ divergence.

Instead, Swamidass emphasizes that “the *aligned* divergence between Chimps and Humans is just ~1.5 [percent]” — seeking to downplay the much larger gap divergence as unimportant.

Joel Duff, a PhD botanist, professor of biology at the University of Akron, who’s also a Christian and a popular theistic evolutionist on YouTube, admits that human and chimp genomes might be only 84 to 85 percent similar. But he states that the non-alignable portion of DNA largely “makes no difference.” He asserts outright regarding the repeats that “it’s not copies of DNA that actually do anything in terms of determining the characteristics of the organism.” He even says that when it comes to repetitive DNA differences, “you don’t need to talk about them when you talk about the differences” because “those differences are not considered very meaningful.” And repetitive DNA differences “don’t represent the real differences between the organisms.” Putting the junk DNA mindset on full display, Duff even says that repetitive DNA differences “don’t even do anything.” Because of this, he asserts that the 14.9 percent genetic difference between humans and chimps is “a meaningless number.” 

Another Christian biologist and evolution-supporter, Zachary Ardern, makes a similar argument. He claims “it’s almost certainly not true that these are differences — not all unaligned regions are real differences — repeat sequences don’t align well.” Elsewhere he uses some helpful analogies for what these repeat differences might look like in terms of written human language. But analogies often break down, and he then argues that adding an extra copy of a repeat might be seen as a “typo” that is not relevant “in terms of functional information.” 

In other words, these critics assume that all the repeat DNA that’s different between humans and chimps is junk, like junk, or largely junk — and having one copy of a repeat is functionally no different from having two copies or three copies or four. Adding more copies is just “cut-and-paste” and it doesn’t make any difference. And because they think it’s junk, they would have us believe that we can dismiss much of the gap divergence genetic differences between humans and chimps as differences that don’t mean anything “in terms of functional information.” But they don’t really know this is true. They don’t know that the different copies of repeats aren’t functionally important.

I’m glad that the critics have clearly stated this objection, because it shows us how evolutionists typically think. They are recapitulating the standard evolutionary presumption that if we don’t know what a genetic element is doing, then we can presume it’s junk. The junk DNA mindset is alive and well. But their presumption is outdated. It cannot stand given the trendline of so much research showing so many different types of functions for so many different types of DNA — including repetitive DNA. 

Against What We Know 

At first blush their argument seems like an “argument from ignorance” where they claim that because we don’t know what this DNA is doing, that therefore it must be junk. Francis Collins warned against this when he said: “I think it was pretty much a case of hubris to imagine that we could dispense with any part of the genome as if we knew enough to say it wasn’t functional.”

But I think this is being a bit too generous. The argument that critics are making is not just an argument from ignorance. It’s an argument that goes against what biology has discovered, because we know that differences in repeat copies can have functional importance. Their casual dismissal of large blocks of divergent DNA simply because it is repetitive directly contradicts scientific knowledge about how repetitive DNA can have function — including function that is directly related to the number of repeat copies. Yet as the Nucleic Acids Research paper shows, when it comes to repetitive DNA, the number of copies is functionally important for determining things like the shape of non-B DNA. The number of copies carries functional information. 

(As an aside with regard to Ardern, informationally speaking, duplicating repeats is not exactly the same as simply duplicating a protein-coding gene. In the latter, you have a second copy of the same gene sequence producing the exact same protein. In such cases, arguably very little new information is generated by duplicating a gene because you’re just generating the same protein, although perhaps you can make more of it due to increased ability to produce gene transcripts. When duplicating repeats, it’s the number of copies that can matter both in terms of the structural shape of the DNA or the length of the RNA that is being transcribed. The way our genomes are designed, duplicating repeats can change the information content in more meaningful ways than simply duplicating a protein-coding gene.)

Other critics have suggested that many of the genetic differences between humans and chimps are meaningless. One scientist wrote, “The key question now is, what is the percentage difference in informative changes? Most of these differences are neutral.” Another biologist wrote, “12.5% im [sic] 6m years is huge! Surely its partly structural alignment artifacts” — in other words, the gap differences merely represent large mutations like insertions, deletions, duplications, inversions, etc. — again not meaningful differences. Ardern alludes to this kind of thinking when he writes that some genome sections “were duplicated or copied multiple times in the lines of descent connecting the two via a common ancestor so don’t have 1:1 alignments.” Here, he is endorsing the standard evolutionary view that major human genetic differences from chimps arose not by intelligent design, but by blind duplication or copying mutations since our supposed common ancestor with chimps. He’s welcome to hold that view. The point is that whether they resulted from random mutations or not, these critics don’t know that these differences aren’t meaningful or important. That’s an evolution-based junk DNA assumption, and it’s an assumption that’s contradicted by much evidence.

The Central Irony

What’s most ironic here is that these critics aren’t disputing that the evidence really does show that humans and chimps are 15 percent genetically different. They’re just trying to find ways to downplay or dismiss those differences. 

So even if their junk-DNA arguments were right (which they aren’t), they don’t change my numbers or my argument: These represent real genetic differences between humans and chimps, and that needs to be recognized regardless of what you think those differences are doing or whether they matter or are junk, etc. 

Strong arguments can be made that the differences entailed in repetitive DNA aren’t “junk”; but even if they were junky differences, that doesn’t affect the percent genetic difference numbers in any way. And that’s what we’re talking about here.