Previous studies have shown that KAT2A could increase the chromatin accessibility of E2F1, DNA Damage Inducible Transcript 3 (DDIT3), and other transcription factors, and form protein complexes with them, and then be recruited to the promoter regions of related genes, consequently enhancing their expression through increasing the acetylation level of H3K9 on these gene-promoting regions and regulating the development of cancer. This evidence concerns the gene DDIT3 and cancer.