Inhibition of LSD1 caused an increase in chromatin availability with strong enrichment in PU.1, C/EBPα, and RUNX1, whereas the loss of C/EBPα or PU.1 led to the resistance of AML cells to LSD1 inhibition both in vitro and in vivo, showing the importance of PU.1 and C/EBPα in modulating the antileukemic efficacy of LSD1 inhibition [59,60,68]. The gene discussed is SPI1; the disease is acute myeloid leukemia.