Epithelial-mesenchymal transition (EMT), a process in which epithelial cells lose cell polarity and transition to a mesenchymal phenotype, plays a critical role during normal development. However, mounting evidence suggests that this process is often abnormally re-activated during cancer recurrence and metastasis. Alternative splicing, a key mechanism for generating protein diversity, is another tightly regulated process that has been shown to be aberrantly altered in cancer. However, whether alternative splicing constitutes a regulatory mechanism in carcinogenesis remains largely unknown.