Data from this and other studies lead us to speculate that U2AF65 could be binding to a multi-stranded nucleic acid structure such as R-loops, D-loops, or G-quartet mRNA in vivo that is mimicked by the purine triplex DNA probe in our study, and that overexpression or increased EMSA binding activity of U2AF65 in tumor tissues could cause deregulation of mRNA splicing and protein isoform expression, such as beta-catenin, that could contribute to colorectal cancer initiation and/or progression. This evidence concerns the gene CTNNB1 and neoplasm.