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Moreover, we can also know which mutations are or are not detectable by static analysis tools.
It should be noted that in some cases observation of the same mutation in two different strains might be due to selection (e.g. if a specific mutation is much more likely to cause the phenotype than other mutations are, or if only a small number of different mutations in the genome are capable of causing the phenotype), rather than due to common inheritance.
Finally, many homeobox gene mutations are (or will be) embryonic or perinatal lethal, making analysis of the development of adult organs particularly challenging.
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In classical evolutionary computing, the recognition that most mutations were or are deleterious meant that mutation rates were kept low.
But it is not clear whether the guilty mutations are inherited, or whether they arise anew in each generation.
Most of the spontaneous mutations are neutral or deleterious, while disadvantage mutations will be discarded, and neutral mutations can still retain.
However, given the disproportionately large size of the FAT genes, it is still unclear if FAT gene mutations are 'passenger' or 'driver' mutations in cancer.
How these embryonic mutations are controlled or remain silent in adults that would later cause site-specific cancers in aging individuals are among important biological knowledge gaps.
Further investigations will be required to determine whether these mutations are drivers or passengers of tumorigenesis.
Of note is that most mutations are truncating or loss-of-function and cause aniridia.
Six of the seven mutations are frameshift or termination codons.
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