Using a human myeloid leukemia cell line containing a gene trap to delete the catalytic SET domain of MLL3 (Fig 6A), we found a significant increase in cell adhesion to the blood plasma and extracellular matrix constituent fibronectin (Fig 6B), as well as significantly enhanced cell migration in response to serum (Fig 6C) upon loss of MLL3 function. This evidence concerns the gene KMT2C and myeloid leukemia.