A study on human prostatic tumors suggested that ANRIL overexpression was mainly accompanied by transcriptional inactivation of the p16-CDKN2A/p15-CDKN2B/p14-ARF locus through cis direct interaction with the two repressive polycomb complexes PRC2 and PRC1 [6]. This evidence concerns the gene CDKN2B and prostate neoplasm.