One possibility may be associated with DNA regulation, as Beclin 1 has been implicated to regulate DNA damage and centrosome stability in colorectal cancer cells.36 Regarding the C-terminal fragment, it has been demonstrated that the C-terminal Beclin 1 sensitized the Ba/F3 cells to apoptosis by driving the release of cytochrome C from mitochondria.12 It is reasonable, therefore, to assume that after cleavage, C-terminal Beclin 1 gains novel function of augmenting cell apoptosis via inducing the release of pro-apoptotic factor from dysfunctional mitochondria. This evidence concerns the gene BECN1 and colorectal cancer.