Indeed, large deletions of this domain in dystrophin result in only a very mild phenotype.

Mutations that alter only the C-terminal of the protein also result in a mild phenotype of the disorder, usually sparing the brain.

This leads to a relatively mild phenotype as receptors are still present on the cell surface (but all must be newly synthesised).

While the previous example suggested that Semaphorins may play pivotal roles in maintaining viable neurons, for the most part Semaphorin knockout animals display mild phenotypes.

This microduplication is more common than the deletion; this might be due to the milder phenotype of the individuals.

By 1999, however, it was apparent that Pin1 knockout mice had a surprisingly mild phenotype, indicating that the enzyme was not required for cell division per se.

Mutations related to the disease have also been noted in exons 7,8, and 9, with milder phenotypes than the other mutations.

Females with full FMR1 mutations may have a milder phenotype than males due to mosaicism resulting from X-inactivation.

Presumably, the genetic defect in these individuals causes less "heterozygous insufficiency," meaning they retain enough gene function to yield a milder phenotype.

Generally this leads to a milder phenotype than in non-mosaic patients with the same disorder.