Based on these findings and known functions of Bif-1 and its splice variants, we hypothesize that SRRM4 mediates the splicing of Bif-1 into CRPC-NE-unique splice variants Bif-1b and Bif-1c, and that these variants are important in helping PCa cells, particularly CRPC-NE cells, to escape apoptosis during CRPC-NE tumor progression. Here, SRRM4 is linked to posterior cortical atrophy.