Mechanisms of FOXM1-dependent senescence elucidated in neoplasms other than myeloma [53] include enhancement of Bmi-1 expression, as seen in the NIH3T3 model [54]; overexpression of miR-370, observed in AML [55]; and inhibition of the CDK4/6-FOXM1 axis by genetic means, such as enforced expression of miR-506 in ovarian cancer [56], or pharmacologic means, such as small-drug CDK inhibition in neuroblastoma [57]. This evidence concerns the gene BMI1 and acute myeloid leukemia.