Consistent with this view, we found that after several days of selective passage in presence of puromycin (designed to maintain stable replicative viral genomes in persistently infected cells), key components of the NF-κB signaling axis were differentially impacted by the virus, even though both MeWo and Mel1700 cells retained their melanoma phenotype, as indicated by sustained expression of Melan-A (Figure 6(d)). This evidence concerns the gene NFKB1 and melanoma.