DDIT4 and neoplasm: For instance, the histone deacetylase HDAC2 could inhibit lncRNA H19 expression by histone H3K27 deacetylation in its promoter via binding with SP1.[39] Oct4, a key stemness transcription factor, transcriptionally activates lncRNA NEAT1 via promoter and lncRNA MALAT1 via enhancer binding to promote cell proliferation and motility, and led to lung tumorigenesis and poor prognosis.[40] Here, we found high enrichment of H3K27ac at the promoter of DDIT4‐AS1 in TNBC cell lines and tumor tissues, and the H3K27ac of DDIT4‐AS1 is positively associated with its expression.