Cytomegalovirus (CMV) belongs to the Betaherpesvirinae subfamily within the Herpesviridae family. CMVs encode a range of genes that target the host immune response. We have recently demonstrated that the m15 locus, encoding the open reading frames (ORF) m14, m15 and m16 expresses five 3’ co-terminal transcripts that span this entire region. A 3` deletion in m15 (K181-3’Δm15), which affects all five transcripts, attenuates MCMV and reduces its dissemination to, and replication in the salivary glands. The product/s of this locus targets host natural killer cells as depletion of asialo-GM1+ cells from CBA mice, but not T cells, rescues this attenuation. In addition, mice infected with this virus show heightened NK cell response, characterised by increased proliferation and production of IFNγ. The exact transcript/s that mediates these effects remains elusive. Paradoxically, deleting the 5’-end of the m15 ORF (K181-5’Δm15), premature termination in the m14 (K181-m14stop), m15 (K181-m15stop) and m16 (K181-m16stop) ORFs failed to recapitulate the phenotype of the original mutant. To dissect this phenotype further, a recombinant MCMV strain was produced in which the entire m14-m16 region was deleted. This MCMV∆m14-m16 recombinant was constructed using a homologous recombination method. A revertant virus, MCMV-Rev was also constructed by two-step allele replacement. Data obtained from in vivo and in vitro testing of these viruses will be discussed in relation to that obtained from the original mutant virus.