Cancer-specific alterations in splice site selection affect genes controlling cellular proliferation (e.g., CD44, Cyclin D1, HER2, and H-Ras), invasion (e.g., CD44, Ron, and MENA), angiogenesis (e.g., VEGF), apoptosis (e.g., Fas, Bcl-x, and caspase-2), and multi-drug resistance (e.g., MRP-1 and p53) (18–20). Here, CD44 is linked to cancer.