MYC and Burkitt lymphoma: This discovery subsequently led to the molecular elucidation of the first gene fusions and translocations in the early 1980s: fusion of ABL1 and BCR resulting from the formation of the Ph chromosome causes constitutive activation of a tyrosine kinase in CML (Figure 3A); and a translocation in ~80% of Burkitt lymphomas that places the MYC gene within a region of highly active promoters belonging to immunoglobulin heavy chain genes causing upregulated and persistent expression of oncogenic MYC [15,92,93,94,95,96,97].