Recent observations indicate that alternative splicing is a common way for eukaryotes to expand their repertoire of gene functions. Studies indicate that approximately 50 percent of human genes exhibit alternative splicing and approximately 15 percent of disease-causing mutations involve aberrant alternative splicing. Different tissues show remarkably different frequencies of alternative splicing, with the brain accounting for approximately 18 percent of such events [Xu et al. (2002). Nucl. Acids Res. 30:3754–3766].

Why might some tissues engage in more alternative splicing than others?