LSD1 expression increases during dysplasia and progressively increases with advanced tumor grade and stage in mouse and human OSCC.12,13 LSD1 promotes cancer stem cells,14 chemoresistance, and relapse.15 LSD1 attenuation inhibits patient-derived xenografts and epidermal growth factor receptor (EGFR) and yes-associated protein (YAP) signaling, which are critical in OSCC.12,16 However, how LSD1-induced epigenetic changes reprogram preneoplasia into OSCC by acting on specific gene networks, phosphoprotein activation, and immune cells remains unclear. The gene discussed is KDM1A; the disease is neoplasm.