Epigeneticmodifications,includingmodificationsonDNA(suchas methylation), and histones (such as acetylation, phosphorylation, and methylation),playpivotalrolesinregulatingcarcinogenesis.1–3Among thesemodificationsonhistones,acetylationandphosphorylationhave beenwellstudiedforalongtime.Incontrast,histonesmethylationwas consideredtobeanirreversibleprocessbefore2004,anddidnotgain great attention until the discovery of histone lysine-specific demethylase 1 (LSD1). LSD1 is a flavin-dependent monoamine oxidase demethylatingmono-anddimethylatedlysines,specificallyhistone3lysine4andhistone3lysine9(i.e.H3K4andH3K9).4 Theconfirmation of the reversibility of histones methylation/demethylation process, openeduparevolutionarynewfieldhadattractedextensivestudiesin thepast10years.5,6 LSD1 uses flavin adenine dinucleotide (FAD) as a cofactor to specificallyremove mono ordimethylatedhistone3 lysine4 (H3K4)and histone3lysine9(H3K9).7,8 Overexpressionofthisenzymewasfound in numerous types of cancer, including lung and bladder cancers,9 neuroblastoma,10 retinoblastoma11 and breast cancer.12 Mechanistic studiesatthemolecularlevelsuggestthatLSD1involvesinpromoting cell proliferation, migration, invasion, and metastasis by epithelial mesenchymal transition (EMT) induction.13 Most recently, scientists unveiledthattheinhibitionofLSD1couldenhancetheimmunogenicity of the tumor and could promote T-cell infiltration.14 Such findings