TFII-I levels were decreased by wild-type infection but not by inORF3 infection in all cell types examined (Fig. 2A); an E1-defective Ad vector that lacked E4-ORF3 expression and contained the cytomegalovirus promoter (Ad-CMV) failed to reduce TFII-I levels in A549 cells, and this ability was restored by incorporating an E4-ORF3 transgene into the vector (HA-E4-ORF3). The gene discussed is GTF2I; the disease is infection.