The finding on Twist1-mediated p16 suppression was parallel to previous report demonstrating that Twist1 overexpression could lead to inhibition of INK4A/ARF activity in cancer cells.39 Similarly, convincing evidence has shown that the Polycomb-group protein Bmi1 controlled cell cycle propagation through repression of p14 and p16 expression.13, 40 In contrast, altered expressional level of Twist1 in leukemic cells did not affect their sensitivity to daunorubucin. This evidence concerns the gene BMI1 and cancer.