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Mutations may increase the likelihood of misfolding by the thermodynamic destabilization of PrPC [15], [16], [17], [18].

Increased expression of JAK2 V617F in patients with homozygous mutations may increase severity of the phenotype in PV [41], perhaps because the mutant and WT JAK2 kinases compete for Epo receptor binding [13].

In one simple case, if selection is intermittent, a haplotype that is driven to fixation during one episode of strong selection may experience subsequent changes during a period of relaxed selection (these mutations may increase, decrease, or not affect resistance), in which case the eventual path taken may include non-favored and/or double mutations.

Cathepsin B is a lysosomal enzyme present in pancreatic acinar cells that appears to be important in protecting the pancreas from premature trypsinogen activation [41], [42], suggesting that CTSB mutations may increase the risk of inappropriate trypsin activity within the acinar cells.

Compensatory mutations may increase substitution numbers at paired sites.

Driver mutations may increase cell division, reduce cell death, or allow cells to overcome density-limiting effects.

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Occasionally, however, a new mutation may increase the organism's adaptation.

If the repeat is present in a healthy gene, a dynamic mutation may increase the repeat count and result in a defective gene.

This may be explained by the "surfing phenomenon", which describes how the frequency of a neutral or positively selected mutation may increase during a demographic expansion, if this mutation is carried by the pioneers [23], [24].

In vitro experiments have shown multi-mutations may increase viral replication efficiency in Lamivudine resistant strains [ 21].

This mutation may increase susceptibility to HPV infection, particularly betaHPVs.

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