Additionally, Wang et al reported that increased levels of lncRNAs-ANRIL in AML patients could significantly induce cancer development and progression through suppression of miR-34a expression, which in turn results in Histone deacetylase 1 (HDAC1) mediated epigenetic downregulation of ASPP2 [36]. The gene discussed is TP53BP2; the disease is acute myeloid leukemia.