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Where would a predicted silent mutation have to be situated to actually result in a loss-of-function mutation (and potentially lead to the onset of disease)?
A. Intron-exon junction/splice site
B. Translational start site
C. Stop codon
D. Anywhere within the exonic sequences
If baroreceptors are primed to detect blood pressure changes and compensate for them, how is it that some patients suffer from chronic hypertension?
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