Furthermore, we performed CRISPR-Cas9-based genetic inactivation of DOT1L in SET2 cells, another JAK2-V617F/TP53 double mutant blast-phase MPN model (Fig. 3C) and were able to confirm that DOT1L-knockout cells showed a significant increase in LSD1-inhibitor sensitivity (Fig. 3D). Here, KDM1A is linked to myeloproliferative neoplasm.