Notably, our previous results from hematopoietic cell infection models indicate that FoxO3a transactivates promoters within intron A of the canonical MIE locus, contributing to the accumulation of IE2 (UL122) mRNA and protein (21, 22); these promoters, iP1 and iP2, were also previously found to contribute to IE2 expression during lytic infection of fibroblasts (31). This evidence concerns the gene IKBKG and infection.