Potentially, the over-activation of MOZ in that could occur in some AML cells (depending on the genetic basis of the gene fusion (35)), and elevated activity on the MIEP is driving this surprising benefit of HCMV infection through production of more IE antigen targets for T cells or indirectly by promoting recruitment of cytotoxic T cells to the tumor environment. This evidence concerns the gene KAT6A and acute myeloid leukemia.