Similar to the megakaryocytic lineage, these mice will not spontaneously develop B-cell leukemia and four additional events found in DS–ALL samples (CRLF2 overexpression, Jak2R683G, Pax5 haploinsufficiency and expression of the dominant negative Ikaros isoform IK6) are required to drive a B-ALL phenotype, although not to full penetrance [74]. This evidence concerns the gene CRLF2 and acute lymphoblastic leukemia.