For example, MYB is required for both RUNX1 transcriptional activity [54, 56], for the ability of a chimeric RUNX1 fusion oncogene to transform hematopoietic cells [54, 57, 58], and RUNX1 can cooperates with MYB to activate ectopic targets through novel MYB binding sites in cancers [53]. This evidence concerns the gene RUNX1 and cancer.