By using a reconstituted mouse model of Myc-induced lymphoma expressing a truncated version of the miR-17/92 cluster in hematopoietic cells, the authors showed an accelerated tumor development probably due to an anti-apoptotic mechanism associated with the suppression of their direct targets, such as inhibitors of proliferation CDKN1A (41), direct regulators of the apoptosis PTEN (42), and BCL2L11 (also known as BIM) (43). This evidence concerns the gene BCL2L11 and neoplasm.