In further support of its tumor suppressor function, RBM25 was previously found to be mutated in breast cancer and to favor the expression of the pro-apoptotic isoform of the BCL2L1 pre-mRNA, the latter via its role in 5ʹ splice site selection in the context of the U1 snRNP20,43,44. Here, BCL2L1 is linked to neoplasm.