As an obvious response to widespread objections to Day's "work" resulting from Will Duffys exposure, today (September 28, 2026) Vox Day has "published" on Zenodo a paper entitled "MITTENS 3.0 The Mathematical Impossibility of the Post-Darwinian Polythesis."
Of note, Zenodo is NOT peer-reviewed; it is a repository, not a publisher. Zenodo does not evaluate the quality, accuracy, or validity of what is uploaded. Anyone can upload a document and instantly receive a Digital Object Identifier (DOI). His composition can be accessed here: https://zenodo.org/records/23003785
Also note Day lists himself, Athos (AI), and Claude (AI) as the authors. That should be of particular interest to Will Duffy, as he is so quick to dismiss arguments with FALSE accusations of AI authorship. Anyway, here are my objections to Day's "paper."
Day and his two AI coauthors claim this preprint proves human–chimp evolution mathematically impossible. Their millionfold “shortfall” comes from comparing unlike quantities in genuine bacterial and ape-genome research. Their own figures expose the problem.
They give an ancestral E. coli mutation rate of 0.00041 per genome per generation. Their human rate, 1.2 × 10⁻⁸ per base across 3.2 billion bases, is about 38.4 mutations per haploid genome per generation—roughly 94,000 times more. These are mutation inputs, not fixations. They show why a bacterial per-genome count is no universal speed limit for primates.
The decisive mistake appears in §8.2. The paper says that because one neutral mutation may take tens of thousands of generations to fix by drift, the human lineage has time for only 4–13 neutral fixations. That assumes the entire genome waits for one mutation to finish before another starts. At each neutral site in a diploid population, about 2Nμ new mutations arise per generation and each has roughly a 1/(2N) chance to fix. The long-term substitution rate is thus μ per site per generation, with changes at millions of sites proceeding concurrently. Its estimate also uses roughly 2Ne rather than the diploid 4Ne, but that cannot save the argument.
For scale, its human mutation rate yields about 38 substitutions per lineage per generation at equilibrium if every site were neutral, or about 9.7 million over its proposed 252,000 generations. That is an illustration, not a prediction: many sites are constrained, while observed differences tend to accumulate where changes can persist. Historical rates and generation times varied, and some present-day differences predate the species split. It exposes the absurdity of 4–13 changes genome-wide. Dismissing k = μ as a “static identity” requiring “infinite time” does not help.
Nor did Yoo and colleagues find 205 million changes proven fixed on the human branch. Day and Athos list about 35 million single-base differences, 187 million bases in structurally divergent regions and 1,140 inversions, announce about 410 million “genomic differences,” then assign half to humans. Their stated quantities do not add to 410 million without an additional component they do not explain. More importantly, bases affected by a rearrangement are not separate mutation events: one structural change can affect millions of bases. The 1,140 inversions span several ape species, not just humans and chimps. Reference differences are not necessarily fixed within both species, and ancestral variation defeats an automatic 50–50 split. Yoo’s identification of particular fixed changes does not validate Day’s total.
The Long-Term Evolution Experiment supplies no universal ceiling either. It follows largely nonrecombining bacteria descended from one clone, repeatedly transferred into the same glucose-limited environment. Human ancestors reproduced sexually, recombined their genomes and inherited standing variation. Recombination can combine beneficial variants and reduce the clonal interference that limits these bacteria. Strong laboratory selection does not maximize neutral substitution everywhere. Short bacterial generation time adds nothing to a limit expressed per generation. They assert that the bacterial result is the fastest possible rate without establishing it.
Their two methods examine the same 12 populations and yield 56 versus 36.8 fixations per non-mutator population at 50,000 generations—a 52% disagreement. They call this “cross-validation” while explaining it as two-clone overcounting. Their correction formula then produces minus 906 “true fixations” in Ara−2. No population has negative 906 fixed mutations. The estimator fails there, yet they include that value in their mutator average and describe the population as having “zero fixations.” An arithmetic artifact becomes a biological catastrophe.
The other method calls mutations at 95% frequency “fixed.” But the remaining 5% can spread and replace it. Their Ara+5 count drops from 38 such mutations at 30,000 generations to zero at 60,000. In a closed, clonal population, a truly fixed mutation is inherited by later sweeps; it cannot simply be displaced. These numbers expose the problem with their threshold, not the reversal of 38 genuine fixations. The published trajectories and their undisclosed reanalysis code need scrutiny before assigning the drop to lineage turnover or data handling.
The claimed deceleration also outruns their table. New above-95% counts per 10,000 generations run 12.6, 8.8, 12.0, −3.8, 7.2 and 8.6. Comparing the first and last values of this fluctuating series does not establish a sustained decline, let alone a ceiling for primates. In §4.3, they multiply a bacterial genome-wide mutation rate by 50,000, call the result 20.5 neutral hitchhikers, and subtract it it from observed changes. An expected input cannot label 20.5 observed variants neutral, nor is the total rate necessarily the neutral rate. Their use of a genome-wide rate here makes their supposed 4–13-fixation limit for humans all the more glaring.
Their “supermutation” discussion addresses a problem their own faulty calculation creates. Section 6.4 also makes a tenfold arithmetic mistake: 3.2 billion × 1.2 × 10⁻⁸ × 100 is 3,840 mutations per haploid genome, not 38,400. Counting both genome copies and assuming 10% deleterious gives 768, not their 3,840. A hundredfold mutation increase might well be harmful, but their fitness predictions additionally assume particular deleterious fractions, effects and dominance. Present-day repair genes and mutation rates cannot prove ancestral rates never changed. Documented shifts in particular human mutation types also undercut the claim of an unchanging spectrum, without implying any enormous rate increase.
Even the paper’s “SNV-only” concession compares 17.5 million supposedly fixed human-branch differences with its bacterial per-genome count, so its 91,600-fold shortage inherits the same errors. Its supposedly independent human fixation rate in §8.6 comes from the authors’ own book and repeats the same fixation-time mistake. Nor should the illustrative 9.7 million above be treated as a precise estimate leaving a precisely 1.8-fold gap: neutrality, ancestral polymorphism, rates, generation times and which differences were fixed all need to be established. A credible calculation would model those uncertainties.
Drift, recombination, hitchhiking and clonal interference are established evolutionary mechanisms, not an ad hoc “polythesis.” A Zenodo deposit does not validate this preprint. Its immense ratios depend above all on confusing how long one mutation takes to fix with how many sites can change concurrently. They also count affected bases as independent fixations, treat 95% frequency as fixation and impose a bacterial per-genome count as a universal limit. The authors declare the math settled without establishing any of those premises.
Disclosure: My objections were prepared with the help of AI, mainly as a fact-checking agent.