Moreover, RBM4 influenced the utilization of the 5′ss of Bcl-x, an apoptosis regulator, inducing a shift from the anti-apoptotic isoform (Bcl-xL) to the pro-apoptotic isoform (Bcl-xS), thereby promoting apoptosis and impeding tumor progression [118, 119]. Here, BCL2L1 is linked to neoplasm.