Additional roles for miR-US5-2 during HCMV infection have been described, including modulation of TGF-β expression through targeting the transcriptional repressor NAB1 (8), mediation of viral assembly compartment formation through targeting components of the endocytic recycling pathway (87), and inhibition of apoptosis through downregulation of Fas (38). This evidence concerns the gene NAB1 and cytomegalovirus infection.