Figure 6G demonstrates that treatment with SNDX-50469 plus OTX015 compared to SNDX-50469 alone for 16 h, while resulting in decline in the protein levels of Ki67, Menin and FLT3, upregulated expressions of p-H2AX, HDM2, Puma, HEXIM1 and cleaved PARP involved in growth inhibition and apoptosis of AML cells [44–46]. The gene discussed is FLT3; the disease is acute myeloid leukemia.