Crucially, SE reactivation by NCD38 eradicates primary MDS-derived leukemia cells with complex karyotypes in vivo, demonstrating that LSD1-mediated SE silencing sustains MDS leukemogenesis, and its reversal offers a potent therapeutic strategy against high-risk MDS (Sugino et al., 2017). Here, KDM1A is linked to myelodysplastic syndrome.