In other words, the deletion of TLE1/4 may relieve the Notch-mediated inhibition of myeloid lineage differentiation and thus promote AML tumorigenesis in synergy with oncogenic events, such as AML1-ETO gene translocation, FOXC1 gene amplification, and FLT3 overexpression (Figure 6) (Kishtagari et al., 2020). The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.