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'''Loss of function mutations''' are typically recessive. When a heterozygote consists of the wild-type allele and the loss-of-function allele, the level of expression of the wild type allele is often sufficient to produce the wild type phenotype. Genetically this would define the loss-of-function mutation as recessive. Alternatively, the wild type allele may not compensate for the loss-of-function allele. In those cases, the phenotype of the heterozygote will be equal to that of the loss-of-function mutant, and the mutant allele will act as a dominant.

'''Loss of function mutations''' are typically recessive. When a heterozygote consists of the wild-type allele and the loss-of-function allele, the level of expression of the wild type allele is often sufficient to produce the wild type phenotype. Genetically this would define the loss-of-function mutation as recessive. Alternatively, the wild type allele may not compensate for the loss-of-function allele. In those cases, the phenotype of the heterozygote will be equal to that of the loss-of-function mutant, and the mutant allele will act as a dominant.

Gain-of-function mutations create a new allele that is associated with a new function. Any heterozygote containing the new allele along with the original wild type allele will express the new allele. Genetically this will define the mutation as a dominant. A primary example of this is the sickle hemoglobin, where the function of the hemoglobin has changed in a way to be not conducive to [[malaria]] [[parasite]]s.  The [[creation science]] organization [[Answers In Genesis]] states the following regarding the mutation that results in sickle cell anemia:

Gain-of-function mutations create a new allele that is associated with a new function. Any heterozygote containing the new allele along with the original wild type allele will express the new allele. Genetically this will define the mutation as a dominant. A primary example of this is the sickle hemoglobin, where the function of the hemoglobin has changed in a way to be not conducive to [[malaria]] [[parasite]]s.  The [[creation science]] organization [[Answers in Genesis]] states the following regarding the mutation that results in sickle cell anemia:

This is good evidence that natural selection plays a part in maintaining a higher frequency of this carrier state. If you are resistant to malaria, you are more likely to survive to pass on your genes. Nevertheless, it is a defect, not an increase in complexity or an improvement in function which is being selected for, and having more carriers in the population means that there will be more people suffering from this terrible [[disease]]. Demonstrating [[natural selection]] does not demonstrate that ‘upward [[theory of evolution|evolution]]’ is a fact, yet many schoolchildren are taught this as a ‘proof’ of evolution.<ref>http://www.answersingenesis.org/creation/v16/i2/anaemia.asp</ref>

{{cquote|This is good evidence that natural selection plays a part in maintaining a higher frequency of this carrier state. If you are resistant to malaria, you are more likely to survive to pass on your genes. Nevertheless, it is a defect, not an increase in complexity or an improvement in function which is being selected for, and having more carriers in the population means that there will be more people suffering from this terrible [[disease]]. Demonstrating [[natural selection]] does not demonstrate that ‘upward [[theory of evolution|evolution]]’ is a fact, yet many schoolchildren are taught this as a ‘proof’ of evolution.<ref>http://www.answersingenesis.org/creation/v16/i2/anaemia.asp</ref>}}

==References==

==References==