It is shown that RBM4 upregulates Mcl-1S expression and enhances the inclusion of exon 11 of IR to generate the IR-B pro-apoptotic isoform in normal tissue, while breast cancer cells decrease expression of Mcl-1S and IR-B through enhanced the phosphorylation of RBM4, acquiring apoptotic resistance [119]. This evidence concerns the gene RBM4 and breast cancer.