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Understanding the functional differences between mutations can also be exploited to determine cellular mechanisms of disease.

It is estimated that about half of the variation in mutation frequencies can be explained by the intrinsic differences in somatic mutation rates between tissues (Lawrence et al., 2013); however, the number of somatic mutations can also vary by over 1000-fold between cancers of the same subtype (Alexandrov et al., 2013; Lawrence et al., 2013).

However, beneficial mutations can also spread 'horizontally' so that they are shared between two (or more) locations in the genome of an individual.

The nature of these mutations can also be characterized by restriction fragment length polymorphisms (RFLP).

Mutations can also allow cancer cells to resist targeted cancer therapy.

Keratin mutations can also cause deformations in the hair, nails, and corneas.

Driver mutations can also occur later in clonal evolution and infer resistant properties that were not present in the initial driver mutation.

And though the focus is understandably on BRCA mutations in women, these mutations can also be carried by men ― and potentially passed on to their children.

Major mutations can also occur.

Furthermore, mitochondrial mutations can also underlie NSHL.

Beneficial mutations can also surf, as can deleterious mutations over finite time spans.