CKM

What it does

Crossing two of them

Its gene carrot

Gene key

horsegenetics.ckm

Priority

82

Alleles

T C

Outcomes

ckm-fast, ckm-mixed, ckm-plain

Coat effect

none — every outcome is a wild type

Default allele

C

Wild population

p(T) = 0.20

Founder draws

1 × nextFloat()

Catalogue entries

1 — it never changes what a horse looks like

The combination table

Same treatment as PDK4: really a marker in a polygenic cluster, modelled here as one atomic gene with an additive weight, because a legible gene a player can breed for beats an accurate sum a player cannot see.

It is the weakest and the rarest of the three speed loci on purpose. Once the obvious gene is fixed there has to be something left to chase, and a locus worth 0.030 at p = 0.20 is exactly the kind of thing a programme finds in its fourth generation rather than its first.

What CKM is

CKM is creatine kinase, M-type — the muscle-type creatine kinase gene, encoding an enzyme expressed mainly in skeletal and cardiac muscle. Its central reaction transfers a phosphate from phosphocreatine to ADP:

phosphocreatine + ADP + H⁺  ⇌  creatine + ATP

That is the phosphagen energy system. At the start of a sprint, a jump take-off, a gallop acceleration or a sudden uphill effort, muscle ATP demand rises almost instantly, and the ATP stored directly in muscle is very limited. CK-M regenerates it locally and fast, acting as an energy buffer and shuttle for extremely high-power contraction over seconds — not as a supply of long-duration aerobic energy.

So CKM is a physiologically plausible muscle-power candidate. Plausibility is not proof that ordinary inherited CKM variants produce a measurable difference in a horse. The annotated equine gene lies on equine chromosome 10 (ECA10), on EquCab3.0 and on the newer TB-T2T assembly. NCBI Gene 100065641

Not a coat gene, not a size gene

CKM is not a coat-colour locus and is not known to affect base colour, any dilution, any white pattern, mane and tail colour, grey, roan, skin pigment or eye colour. Those come from MC1R, ASIP, KIT, STX17, PMEL, TBX3 and their neighbours. The mod agrees — every CKM outcome is marked wildType.

Nor is it an established size or conformation gene: not withers height, body mass, frame, bone length, neck or shoulder or croup or limb angle, hoof or joint size, or muscle mass in the way the “speed gene” label sometimes implies. The best-supported body-size region in horses is on ECA3 near LCORL and NCAPG; a 2024 study of 2,709 German Warmblood mares found the ECA3 region accounted for a very large share of the genetic signal for withers height, and CKM — on ECA10 — was not implicated. PMC11177368

Speed — the claim, and what happened to it

The horse-specific CKM claim traces to a 2010 candidate-gene study of Thoroughbreds. Researchers found novel SNPs in ACTN3, CKM and COX4I2, then compared “elite” Thoroughbreds against horses that had never won. Three SNPs in CKM/COX4I2 were nominally significant in the initial sample.

The associations were then not validated in an additional independent sample of 130 horses, and when all samples were combined, only a COX4I2 variant retained a reported association. PMID 21059062

The SNP usually quoted from that work is CKM g.15884567G>A in EquCab2.0 coordinates, with the original work and its patent materials proposing that the A allele — especially A/A — might be enriched among elite performers. WO2010029527A1 It is an exploratory association that did not replicate, not an established marker.

A later study tested the same variant in Quarter Horses — 296 from racing lines and 68 from cutting lines. The marker was polymorphic, and there was no significant association with line type or with the extreme racing-performance groups compared. The authors’ conclusion was explicit: the tested CKM SNP was not related to racing performance in Quarter Horses. J Equine Vet Sci

Jumping

No direct evidence that CKM genotype predicts scope, jump height, bascule, carefulness, technique, take-off distance, landing mechanics, show-jumping results or eventing performance. Its energy role makes a tiny contribution to explosive hindlimb contraction at take-off hypothesisable, and that is all it is.

Equine jumping GWAS work has identified QTL on other chromosomes, near genes including RYR2, ACTA1 and ACTN2 — more directly tied to muscle calcium signalling and muscle structure. That does not prove those genes “cause jumping”; it shows the current literature does not name CKM as a validated jumping locus. Front. Genet. 11:448

Jumping is a stack of interacting layers: limb and back conformation; muscle force, elastic recoil, coordination and balance; canter quality and adjustability; vision, temperament, learning and rider interaction; training history, conditioning, injury, footing, course design and management. A single SNP would be expected, at most, to contribute very little among all of that. The mod gives CKM no jump effect at all, which is the right call.

If it did anything, it would be this kind of speed

Were a functional CKM difference ever shown to matter, the plausible phenotype is very-short-duration, high-rate ATP turnover: the first strides from a start, sudden acceleration, brief maximal galloping, a jump take-off, fast muscle-force transients. It is much less plausible that CKM alone governs sustained aerobic capacity or long-distance racing, which depend far more on oxygen delivery, mitochondrial density and function, cardiovascular capacity, thermoregulation, glycogen and fat metabolism, biomechanics and training adaptation. That is biochemical reasoning, not evidence about real horses.

Inheritance

An ordinary autosomal gene on ECA10 — not sex-linked, not mitochondrial. For a single biallelic SNP the genotypes are the usual three, transmitted the usual way, and two heterozygotes give 25% / 50% / 25%.

That the genotypes segregate simply does not mean the phenotype follows a simple dominant or recessive pattern. There is no validated, breed-general answer to whether the proposed elite allele is dominant, recessive or additive. If CKM has any population-level effect at all it could be additive (each copy a small shift), dominant (one copy as good as two), recessive (two copies needed), overdominant (heterozygotes unlike either homozygote), context-dependent (visible only in a breed, distance, training environment or ancestry group), or not causal at all — the SNP may simply have been linked to a nearby causal variant in the original population, or the association may have been chance.

Breeds and frequency

So the honest answer to “which breeds, and how common?” is: documented as polymorphic in Thoroughbreds and Quarter Horses; no defensible percentage available for Thoroughbreds, Quarter Horses, Warmbloods, Arabians, Standardbreds or anything else. And “found in a breed” is not “important in that breed”, which is not “predictive within that breed”.

The mod uses p(T) = 0.20, which has no published counterpart to be checked against. It was chosen so that the locus is the second-rarest of the three speed genes — a gameplay ordering, not a population measurement.

Health

There is no established equine CKM variant causing a recognised inherited health syndrome, growth disorder, orthopaedic disease or performance-limiting muscle disease. That does not make CKM irrelevant to health: CK-M activity is central to muscle energetics, and serum creatine kinase is a standard clinical blood biomarker of muscle damage. But that is an enzyme measurement, not evidence that the SNP from an old performance panel causes muscle disease.

What this means for the gene as implemented

Known. CKM encodes a major skeletal-muscle energy-buffering enzyme; it is on ECA10; a historical Thoroughbred candidate-gene study reported an initial association with elite racing status; that signal failed independent validation, with the combined analysis retaining COX4I2 rather than CKM; the marker was polymorphic but unassociated with line or performance in Quarter Horses; and CKM has no validated association with coat, height, build, jumping or any hereditary disease.

Speculative. That a CKM allele improves brief maximal power enough to change race results; that it determines acceleration or explosive take-off; that A/A at g.15884567G>A marks elite Thoroughbred potential; that a CKM test can guide breeding, purchasing, discipline choice or training; and that CKM meaningfully affects muscle mass or conformation.

So the mod ships a speed locus the real literature does not support. That is a deliberate trade and it is worth naming rather than burying: the mod wants three legible speed genes of different sizes so a breeding programme has a gradient with a long tail, and CKM is the smallest of the three precisely because it is the least defensible. The alternative designs were to drop it (leaving two speed loci and a much shorter programme) or to model the real polygenic architecture (which a player cannot see or breed for). Neither is better; both are honest. What is not honest is letting a page imply the biochemistry settles the genetics. It does not — and the same caution applies with less force to PDK4, which is the other marker-in-a-cluster modelled as an atomic gene here.