This led us to hypothesize that PV propagation in illegitimate hosts might depend on constitutively active PDK1/PKC/PKB signaling, since some PV-permissive human cancer cells (e.g. NCH149) display, irrespectively of infection, significantly higher levels of PDK1phosphoS241 and PKBphosphoT308 than normal cells, together with PKCη/Rdx-induced phosphorylation of PDK1:S135 (Fig. 4). The gene discussed is RDX; the disease is cancer.