Given the tumor suppressor role of p300 in multiple MDS models, we next examined whether chemical modulation of p300 KAT activity using an inhibitor (A-485; refs. 37, 38) and an activator (I-CBP112; ref. 39) would similarly affect the self-renewal and proliferation of Tet2-deficient HSPCs (Figure 6A). Here, EP300 is linked to neoplasm.