It is likely that the pronounced anti-tumor effect of Hsp90 inhibitors is due to the downregulation of multiple targets: LANA, which is essential for viral maintenance [17], cdc2, Akt, which transduces paracrine and autocrine growth signals in PEL, KS and other cancers [51], NFkB activators [15], ephrin-B2, and EphA2, which support KSHV re-infection of endothelial cells and thus tumor maintenance and even targets of surface bound Hsp90 [16]. Here, NFKB1 is linked to infection.