Necroptosis was originally identified as an alternative cell death program activated when caspase was blocked and is now also recognized as cellular defense mechanism against infection, including dsDNA viruses.36,37 Expression of both RIP3 (Figure 5a), the key mediator of necroptosis38 and the TNF receptor (Tnfrsf1a, Figure 5b), an activator of the necrosome complex,38 were increased only in cells treated with p19Arf+IFNβ. This evidence concerns the gene IFNB1 and infection.