Cancer cells often exhibit dysregulated splicing patterns, leading to the expression of oncogenic isoforms and the suppression of tumor suppressor isoforms. For example, the splicing of the gene BCL2L1 can result in either a pro-apoptotic or anti-apoptotic protein, depending on which exons are included. In many cancers, the anti-apoptotic variant is predominantly expressed, enabling the cancer cells to evade programmed cell death.
