Recently, it has been demonstrated that KRAS mutations confer apoptosis resistance in CRC via upregulation of Bcl-xL underpinning the role of the protein as a potential target.24, 25 Furthermore, Bcl-xL has been identified as a critical survival factor utilizing frequent genomic alterations in a subset of CRCs.26 This evidence concerns the gene BCL2L1 and colorectal carcinoma.