Those phenotypes are mediated via RNF5 interaction with the chromatin remodeling protein RBBP4, which results in its non-canonical (K29 topology) ubiquitination that promotes RBBP4 recruitment to specific gene promoters (among them, ANXA1, NCF1, and CDKN1A), and a concomitant regulation of genes implicated in AML maintenance. The gene discussed is CDKN1A; the disease is acute myeloid leukemia.