Inversion or translocation of chromosome 3 drives AML through enhancer dysregulation. An enhancer on chromosome 3 normally drives expression of the TF GATA2 in hematopoietic progenitor cells. Elsewhere on chromosome 3 is the TF EVI1. Structural abnormalities of chromosome 3 found in one type of AML, such as inv(3) or t(3;3), lead to the movement of this enhancer away from GATA2, resulting in loss of expression, and nearer to EVI1, driving its expression. A series of studies of these chromosome 3 abnormalities have determined that ectopic transcription of EVI1 is sufficient to drive AML, whereas concomitant loss of GATA2 expression accelerates this process.