Mutations in the low-density lipoprotein receptor (LDLR) gene are a primary
cause of familial hypercholesterolemia. One such mutation is a SNP in exon 12
of the \(L D L R .\) In premenopausal women, but not in men or postmenopausal
women, this SNP leads to skipping of exon 12 and production of a truncated
nonfunctional protein. It is hypothesized that this SNP compromises a splice
enhancer [Zhu et al. (2007). Hum Mol Genet. \(16: 1765-1772\) ]. What are some
possible ways in which this SNP can lead to this defect, but only in
premenopausal women?