AML1‐ETO triggers the silencing of miR‐193a and in contrast, miR‐193a decreases AML1‐ETO expression via targeting its binding sites, suggesting that a feedback circuitry is formed in AML cells bearing AML1‐ETO.32 It is possible that MLT‐induced degradation of AML1‐ETO disrupts the feedback circuitry and increases the expression of miR‐193a. The gene discussed is RUNX1; the disease is acute myeloid leukemia.