Collectively, these data purport a model whereby epigenetic silencing of MEIS1/2 in prostate tumors allows oncogenic AR/HOXB13 interactions; HOXB13 mutations could modify the affinity of HOXB13 for AR vs. MEIS, diminish MEIS/HOXB13 transcriptional regulation of tumor suppressive genes such as DCN, or enable increased oncogenic MEIS-HOXA9/10 interactions. This evidence concerns the gene HOXA9 and neoplasm.