We hypothesize that RNASEH2A promotes NPC genesis through IKKi signaling, inhibition of RNASEH2A and/or IKKi would be a high-efficient way to prevent and block NPC development. We will investigate whether genetically and pharmaceutically inhibiting RNASEH2A and/or IKKi blocks NPC development in mouse models, and whether the tumor-promoting function of RNASEH2A is dependent on IKKi signaling. We firmly believe that our studies will lead to development of novel strategies for the treatment and prevention of human NPC.