These differentially spliced exons include the AR-ESRP2-controlled alternative exons in the DOCK7 and RPS24 genes (both of which were excluded in prostate tumours compared to normal prostate tissue); and the alternative exons in the MINK1 and MAP3K7 genes (each of which had increased levels of splicing inclusion in prostate tumours compared to normal tissue). This evidence concerns the gene AR and prostate neoplasm.