Moreover, DOT1L inhibitor SYC-522, when in combination with mitoxantrone, a classical chemotherapeutic agent, can significantly enhance chemotherapy efficacy by inhibiting the DNA damage response, thereby increasing the sensitivity of leukemic cells to chemotherapy, while SYC-522 alone reduces the clonogenic capacity of MLL-rearranged AML cells by only approximately 50% (Liu et al., 2014). The gene discussed is DOT1L; the disease is acute myeloid leukemia.