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). The gene discussed is FOXC1; the disease is acute myeloid leukemia.