MGA truncating mutations are also frequently observed in CBF-AMLs and have been shown to cooperate with RUNX1::RUNX1T1 to accelerate leukemogenesis in preclinical models, supporting a tumor-suppressor role (23).Studies have confirmed that in mouse hematopoietic cells with MGA deletion, the expression of RUNX1::RUNX1T1 results in more aggressive AML with a significantly shortened latency period (24). Here, RUNX1 is linked to neoplasm.