. In shows, they normally are classed in two sections: competition height A, and under; and competition height B, over . New Forest ponies should be of riding type, workmanlike, and strong in conformation, with a sloping shoulder and powerful hindquarters; the body should be deep, and the legs straight with strong, flat bone, and hard, rounded hooves. Larger ponies, although narrow enough in the barrel for small children to ride comfortably, are also capable of carrying adults. Smaller ponies may not be suitable for heavier riders, but they often have more show quality. The New Forest pony has free, even gaits, active and straight, but not exaggerated, and is noted for sure-footedness, agility, and speed. The ponies are most commonly bay, chestnut, or grey. Few coat colours are excluded: piebald, skewbald, and blue-eyed cream are not allowed; palomino and very light chestnut are only accepted by the stud book as geldings and mares. Blue eyes are never accepted. White markings on the head and lower legs are allowed, unless they appear behind the head, above the point of the hock in the hind leg, or above the metacarpal bone at the bend in the knee in the foreleg. Ponies failing to pass these standards may not be registered in the purebred section of the stud book, but are recorded in the appendix, known as the X-register. The offspring of these animals may not be registered as purebred New Forest ponies, as the stud book is closed and only the offspring of purebred-approved registered ponies may be registered as purebred. New Forest ponies have a gentle temperament and a reputation for intelligence, strength, and versatility. On the whole, they are a sturdy and hardy breed. The one known hereditary genetic disorder found in the breed is congenital myotonia, a muscular condition also found in humans, dogs, cats, and goats. It was identified in the Netherlands in 2009, after a clinically affected foal was presented to the Equine Clinic of Utrecht University. DNA sequencing revealed that the affected foal was homozygous for a missense mutation in the gene encoding CLCN1, a protein which regulates the excitability of the skeletal muscle. The mutated allele was found in both the foal's parents, its siblings, and two other related animals, none of whom exhibited any clinical signs. The researchers concluded that the condition has an autosomal recessive mode of inheritance, whereby both parents have