FOXC1 overexpression is common in AML with wild-type AML1 (Han et al., 2017; Simeoni and Somervaille, 2021), where TLE3 forms a complex with wild-type AML1, FOXC1, and HDAC1, thereby blocking the terminal differentiation of myeloid cells and leading to AML development (Figure 6) (Simeoni and Somervaille, 2021). Here, TLE3 is linked to acute myeloid leukemia.