In contrast to TR, the RUNX1‐ETO (RE) fusion which is found in many cases of AML induces a potent SLGA in primary human foreskin fibroblasts.24 However, the t(8;21) fusion also generates a minor spliced variant of RE lacking two C‐terminal ETO repressor domains that is much more potently leukemogenic in mouse models26 (Figure 3A). The gene discussed is RUNX1T1; the disease is acute myeloid leukemia.