Our results supported a novel hypothesis that cellular stresses, including adenovirus infection and exposure to TNF-α, contributed to sustained activation of NFκB signaling through a non-canonical EGFR pathway associated with phosphorylation of a Thr254-Pro motif in NFkB-p65, which is a known Pin1 substrate that is unmasked by IκB degradation [54]. This evidence concerns the gene EGFR and adenoviridae infectious disease.